Results of lignin isolation at variations in bagasse size and NaOH concentrations.
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:{caption:"IntechOpen Maintains",originalUrl:"/media/original/113"}},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"5277",leadTitle:null,fullTitle:"Challenges in Parkinson's Disease",title:"Challenges in Parkinson's Disease",subtitle:null,reviewType:"peer-reviewed",abstract:"Parkinson's disease is a common neurological disease and affects 2% population of more than 65 years of age and 5% more than 85 years of age. Pathomechanism of this disease is still not fully understood. This book is a sum up of knowledge on the genetic factors and neuronal death mechanisms induced by excitotoxic and inflammatory agents. The authors summarize the pathophysiology observed both in patients with Parkinson's disease and in experimental models. The book also contains the latest views on drug therapy used in the treatment of parkinsonism and other therapeutic approaches for Parkinson's disease. The book ''Challenges in Parkinson's Disease'' was made as a compendium on contemporary challenges in Parkinson's disease.",isbn:"978-953-51-2464-1",printIsbn:"978-953-51-2463-4",pdfIsbn:"978-953-51-7291-8",doi:"10.5772/61880",price:139,priceEur:155,priceUsd:179,slug:"challenges-in-parkinson-s-disease",numberOfPages:400,isOpenForSubmission:!1,isInWos:1,isInBkci:!1,hash:"ec247c295eeed9e8c8ab48a63b0b94c1",bookSignature:"Jolanta Dorszewska and Wojciech Kozubski",publishedDate:"August 24th 2016",coverURL:"https://cdn.intechopen.com/books/images_new/5277.jpg",numberOfDownloads:35073,numberOfWosCitations:20,numberOfCrossrefCitations:18,numberOfCrossrefCitationsByBook:2,numberOfDimensionsCitations:31,numberOfDimensionsCitationsByBook:2,hasAltmetrics:1,numberOfTotalCitations:69,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 9th 2015",dateEndSecondStepPublish:"November 30th 2015",dateEndThirdStepPublish:"March 5th 2016",dateEndFourthStepPublish:"June 3rd 2016",dateEndFifthStepPublish:"July 3rd 2016",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"31962",title:"Dr.",name:"Jolanta",middleName:null,surname:"Dorszewska",slug:"jolanta-dorszewska",fullName:"Jolanta Dorszewska",profilePictureURL:"https://mts.intechopen.com/storage/users/31962/images/4731_n.jpg",biography:"Editor, Professor Jolanta Dorszewska is Chief of Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences (PUMS), Poznan, Poland. Prof. Dorszewska graduated from PUMS, (M.Sc., Pharmacy, 1987), Ph.D. degree obtained at PUMS, (1996), D.Sc. in Medical Sciences at PUMS, (2004) and Full Prof., (2016). Between the years 1999 and 2000 she worked as a Research Scientist at the Institute for Basic Research in Developmental Disabilities, New York, USA.\r\nProf. Dorszewska is an author and co-author of about 100 papers (e.g. Oncotarget, Curr. Alzheimer Res., Seizure) mainly concerning the pathophysiology of Parkinson’s and Alzheimer’s diseases as well as epilepsy and migraine. She is also a co-author and co-editor of books on genetic and biochemical factors in neurological diseases. \r\nProf. Dorszewska was also a Guest Editor of two Theme Issue in Current Genomics (2014, 2013), and a member of Editorial Board in Advances in Alzheimer’s Disease and Austin Alzheimer’s and Parkinson’s Disease (USA). Prof. Dorszewska is a member of the Commission of Neurochemistry of Neurological Sciences, Polish Academy of Science and Polish Association of Neuropathologists, as well as International Association of Neuropathologists.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"10",totalChapterViews:"0",totalEditedBooks:"3",institution:{name:"Poznan University of Medical Sciences",institutionURL:null,country:{name:"Poland"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"83372",title:"Prof.",name:"Wojciech",middleName:null,surname:"Kozubski",slug:"wojciech-kozubski",fullName:"Wojciech Kozubski",profilePictureURL:"https://mts.intechopen.com/storage/users/83372/images/system/83372.jpg",biography:"Prof. Wojciech Kozubski, MD, PhD is the Head of the Department of Neurology, University of Medical Sciences in Poznan, Poland.\nHe graduated from Medical School in Lodz in 1980. In 1983 he received his PhD and in 2002, his professorship.\nFrom 1987 to 1991, he was awarded a scholarship from the Academic Unit of Neuroscience, University of London, Department of Neurology, University of Tel-Aviv and the Department of Neurology, University of Trondheim.\nHe is an author and co-author of over 300 papers concerning the migraine and related headaches, stroke, and dementia. He is the editor of the handbook of clinical neurology for neurologists, the handbook for medical students, monographs on brain tumours, affective diseases of nervous system and therapy in neurology. \nFrom 2011 to 2014, he was the President of the Polish Neurological Society.",institutionString:"Poznań University of Medical Sciences",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"8",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Poznan University of Medical Sciences",institutionURL:null,country:{name:"Poland"}}},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1056",title:"Neurology",slug:"neurology"}],chapters:[{id:"51328",title:"Introductory Chapter - Genetic and Biochemical Factors in Parkinson’s Disease",doi:"10.5772/64216",slug:"introductory-chapter-genetic-and-biochemical-factors-in-parkinson-s-disease",totalDownloads:1480,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,abstract:null,signatures:"Jolanta Dorszewska and Wojciech Kozubski",downloadPdfUrl:"/chapter/pdf-download/51328",previewPdfUrl:"/chapter/pdf-preview/51328",authors:[{id:"31962",title:"Dr.",name:"Jolanta",surname:"Dorszewska",slug:"jolanta-dorszewska",fullName:"Jolanta Dorszewska"},{id:"83372",title:"Prof.",name:"Wojciech",surname:"Kozubski",slug:"wojciech-kozubski",fullName:"Wojciech Kozubski"}],corrections:null},{id:"50469",title:"Genetics of Parkinson’s Disease: The Role of Copy Number Variations",doi:"10.5772/62881",slug:"genetics-of-parkinson-s-disease-the-role-of-copy-number-variations",totalDownloads:1655,totalCrossrefCites:1,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Parkinson’s disease (PD), the second most common progressive neurodegenerative disorder, was long believed to be a non-genetic sporadic origin syndrome. The identification of distinct genetic loci responsible for rare Mendelian forms of PD has represented a revolutionary breakthrough, allowing to discover novel mechanisms underlying this debilitating still incurable condition. Along with single-nucleotide polymorphisms (SNPs), other kinds of DNA molecular defects have emerged as significant disease-causing mutations, including large chromosomic structural rearrangements and copy number variations (CNVs). Due to their size variability and to the different sensitivity and resolution of detection methodologies, CNVs constitute a particular challenge in genetic studies and the pathogenetic or susceptibility impact of specific CNVs on PD is currently under debate. In this chapter, we will review the current literature and bioinformatic data describing the involvement of CNVs on PD pathobiology. We will discuss the recently highlighted role of PARK2 heterozygous CNVs, the possible common founder effects of PD gene rearrangements and the importance to map genetic breakpoints. We will also add a summary about the current available molecular methods and bioinformatics web resources to detect and interpret CNVs. Assessing the global genome-wide burden of large CNVs and elucidating the role of de novo rare structural variants on PD may reveal new candidate genes and consequently ameliorate diagnosis and counselling of mutations carriers.",signatures:"Valentina La Cognata, Velia D’Agata, Francesca Cavalcanti and\nSebastiano Cavallaro",downloadPdfUrl:"/chapter/pdf-download/50469",previewPdfUrl:"/chapter/pdf-preview/50469",authors:[{id:"180809",title:"Dr.",name:"Sebastiano",surname:"Cavallaro",slug:"sebastiano-cavallaro",fullName:"Sebastiano Cavallaro"},{id:"183182",title:"MSc.",name:"Valentina",surname:"La Cognata",slug:"valentina-la-cognata",fullName:"Valentina La Cognata"},{id:"183184",title:"Dr.",name:"Francesca",surname:"Cavalcanti",slug:"francesca-cavalcanti",fullName:"Francesca Cavalcanti"},{id:"186093",title:"Prof.",name:"Velia",surname:"D'Agata",slug:"velia-d'agata",fullName:"Velia D'Agata"}],corrections:null},{id:"50586",title:"Mechanisms for Neuronal Cell Death in Parkinson’s Disease: Pathological Cross Talks Between Epigenetics and Various Signalling Pathways",doi:"10.5772/63103",slug:"mechanisms-for-neuronal-cell-death-in-parkinson-s-disease-pathological-cross-talks-between-epigeneti",totalDownloads:1599,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Parkinson’s disease (PD) is an incapacitating neurodegenerative disorder affecting the population over the age of 65 years. Clinically, most patients present with the symptoms of bradykinesia, resting tremor, rigidity, and postural instability. A number of patients also suffer from autonomic, cognitive, and psychiatric disturbances. The symptoms of PD result from the selective loss of dopaminergic (DA) neurons in the substantia nigra (SNc) pars compacta. However, the exact molecular mechanism that causes this cell death still remains elusive. The cross talk between various molecular signals facilitates the cell to undergo developmental and differentiation programs with such tantalizing accuracy. In recent years, epigenetic mechanisms have advanced as a regulatory driver of processes such as signal transduction, cell cycle control, and stress response. These include DNA methylation, histone modifications, and small RNA-mediated mechanisms. Increasing evidence suggests that epigenetic mechanisms play a major role in the pathogenesis of PD. Researchers are now working to comprehend the therapeutic promises of epigenetic molecules to offset age-related neurodegenerative diseases. In this chapter, we focus on some examples of the cross talk between epigenetic processes and various signal transduction pathways that underlie the pathogenesis of PD.",signatures:"S Meenalochani, ST Dheen and SSW Tay",downloadPdfUrl:"/chapter/pdf-download/50586",previewPdfUrl:"/chapter/pdf-preview/50586",authors:[{id:"183242",title:"Associate Prof.",name:"Samuel Sw",surname:"Tay",slug:"samuel-sw-tay",fullName:"Samuel Sw Tay"},{id:"184878",title:"Dr.",name:"Meenalochani",surname:"Sivasubramanian",slug:"meenalochani-sivasubramanian",fullName:"Meenalochani Sivasubramanian"},{id:"184879",title:"Prof.",name:"Thameem",surname:"Dheen",slug:"thameem-dheen",fullName:"Thameem Dheen"}],corrections:null},{id:"51327",title:"Inflammation: Role in Parkinson's Disease and Target for Therapy",doi:"10.5772/63164",slug:"inflammation-role-in-parkinson-s-disease-and-target-for-therapy",totalDownloads:1607,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,abstract:"Evidence is now overwhelming that inflammation is a central process in the pathogenesis of progressive Parkinson's disease (PD). The hallmark of this neuroinflammation is the activation of microglial cells and the secondary role of adaptive immunity in both the familial and idiopathic forms of PD, leading to the loss of dopamine‐producing cells within the Substantia nigra. This activation is characterized by the oxidative stress response, production of inflammatory mediators, recruitment and activation of immune effector cells which create a toxic environment for dopaminergic neurons, and in forming a continuous cycle of inflammatory responses that result in chronic neuroinflammation and progressive neurodegeneration. This chapter focuses on the different components of the inflammatory response that are involved in Dopamine‐neurodegeneration, the evidence for inflammation in different forms of PD, and the role of inflammation in the various animal models of PD. Finally, we provide current evidence that targeting this inflammation with a number of anti‐inflammatory therapies can be an effective way to halt the progression of chronic neuroinflammation‐induced PD.",signatures:"Patrick Flood, Naik Arbabzada and Monika Sharma",downloadPdfUrl:"/chapter/pdf-download/51327",previewPdfUrl:"/chapter/pdf-preview/51327",authors:[{id:"181605",title:"Prof.",name:"Patrick",surname:"Flood",slug:"patrick-flood",fullName:"Patrick Flood"},{id:"183202",title:"MSc.",name:"Monika",surname:"Sharma",slug:"monika-sharma",fullName:"Monika Sharma"},{id:"183203",title:"BSc.",name:"Naik",surname:"Arbabzada",slug:"naik-arbabzada",fullName:"Naik Arbabzada"}],corrections:null},{id:"50694",title:"Chronic Inflammation Connects the Development of Parkinson’s Disease and Cancer",doi:"10.5772/63215",slug:"chronic-inflammation-connects-the-development-of-parkinson-s-disease-and-cancer",totalDownloads:1580,totalCrossrefCites:2,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Increasing number of genetic studies suggest that the pathogenesis of Parkinson’s disease (PD) and cancer may involve similar genes, pathways, and mechanisms. The differences in the pathological and cellular mechanisms, and the associated genetic mutations, may result in two such divergent diseases. However, the links between the molecular mechanisms that cause PD and cancer remain to be elucidated. This article appraises the overlapping molecular features of these diseases and discusses the implications for prevention and treatment. We propose that chronic inflammation (CI) in neurons and tumors contributes to a microenvironment that favors the amassing of DNA mutations and facilitating disease formation. CI may therefore play a key role in the development of PD and cancer, and provide a link between these two diseases.",signatures:"Zhiming Li and Chi-Meng Tzeng",downloadPdfUrl:"/chapter/pdf-download/50694",previewPdfUrl:"/chapter/pdf-preview/50694",authors:[{id:"181894",title:"Prof.",name:"Chi-Meng",surname:"Tzeng",slug:"chi-meng-tzeng",fullName:"Chi-Meng Tzeng"},{id:"185049",title:"Dr.",name:"Zhiming",surname:"Li",slug:"zhiming-li",fullName:"Zhiming Li"}],corrections:null},{id:"50932",title:"Is Chronic Systemic Inflammation a Determinant Factor in Developing Parkinson’s Disease?",doi:"10.5772/62955",slug:"is-chronic-systemic-inflammation-a-determinant-factor-in-developing-parkinson-s-disease-",totalDownloads:1603,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"The etiology of Parkinson’s disease (PD) is complex and involves numerous risk factors as environmental and hereditary. Nevertheless, recent studies have established that systemic inflammation and neuroinflammation are both present in the prodromal phase and sustained during the progression of the disease. Evidence suggests that the activation of the peripheral immune system exacerbates the brain inflammatory response, which may initiate or enhance neurodegenerative processes. Understanding the impact of chronic systemic inflammation in the neuroinflammation and the progression of the disease will provide a broader view of the etiology and pathology of PD. In this chapter, we review the role of the chronic systemic inflammation in neuroinflammation and its effect on PD, considering cell types, molecular, and inflammatory mediators that predispose to the development of the disease.",signatures:"Perla Ugalde-Muñiz, Jesús Pérez-H and Anahí Chavarría",downloadPdfUrl:"/chapter/pdf-download/50932",previewPdfUrl:"/chapter/pdf-preview/50932",authors:[{id:"181865",title:"Dr.",name:"Anahí",surname:"Chavarría",slug:"anahi-chavarria",fullName:"Anahí Chavarría"},{id:"186120",title:"MSc.",name:"Perla",surname:"Ugalde-MUñiz",slug:"perla-ugalde-muniz",fullName:"Perla Ugalde-MUñiz"},{id:"186121",title:"Dr.",name:"Jesús",surname:"Pérez-H",slug:"jesus-perez-h",fullName:"Jesús Pérez-H"}],corrections:null},{id:"50533",title:"Disorders of Sleep and Motor Control During the Impaired Cholinergic Innervation in Rat – Relevance to Parkinson’s Disease",doi:"10.5772/62949",slug:"disorders-of-sleep-and-motor-control-during-the-impaired-cholinergic-innervation-in-rat-relevance-to",totalDownloads:1352,totalCrossrefCites:3,totalDimensionsCites:6,hasAltmetrics:0,abstract:"The medical profession has been generally very slow to acknowledge the importance of sleep medicine and sleep research. Disorders of sleep are related to anxiety, many mental and neurodegenerative diseases, cardiovascular and respiratory disorders, and obesity.",signatures:"Jasna Saponjic, Jelena Petrovic, Jelena Ciric and Katarina Lazic",downloadPdfUrl:"/chapter/pdf-download/50533",previewPdfUrl:"/chapter/pdf-preview/50533",authors:[{id:"182938",title:"Prof.",name:"Jasna",surname:"Saponjic",slug:"jasna-saponjic",fullName:"Jasna Saponjic"},{id:"183348",title:"Ph.D.",name:"Jelena",surname:"Petrovic",slug:"jelena-petrovic",fullName:"Jelena Petrovic"},{id:"183349",title:"Ms.",name:"Katarina",surname:"Lazic",slug:"katarina-lazic",fullName:"Katarina Lazic"},{id:"183350",title:"M.Sc.",name:"Jelena",surname:"Ciric",slug:"jelena-ciric",fullName:"Jelena Ciric"}],corrections:null},{id:"50470",title:"Cognitive Impairment in Parkinson’s Disease: Historical Review, Past, and Present",doi:"10.5772/62888",slug:"cognitive-impairment-in-parkinson-s-disease-historical-review-past-and-present",totalDownloads:1270,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Parkinson’s disease (PD) is a neurodegenerative disorder of unknown etiology, not only characterized by motor signs but also by non-motor symptoms, including neuropsychiatric and cognitive dysfunction. The results obtained in the last decades show that the cognitive changes in PD are heterogeneous; impairment in different cognitive domains such as attention, executive, language, memory, and visuospatial functions can be present even in the early stages of the disease. Mild cognitive impairment is frequent in non-demented PD patients and is considered as a risk factor for the development of dementia. As a response to the heterogeneity of cognitive impairment associated with PD, the Movement Disorders Society has recently developed formal diagnostic criteria for mild cognitive impairment and dementia associated with PD. In the present chapter, the authors have conducted a revision of cognitive impairment in PD, describing the results obtained in numerous investigations, from the first studies in the1970s to the advances of the last few years.",signatures:"Ivan Galtier, Antonieta Nieto and Jose Barroso",downloadPdfUrl:"/chapter/pdf-download/50470",previewPdfUrl:"/chapter/pdf-preview/50470",authors:[{id:"182255",title:"Dr.",name:"Iván",surname:"Galtier",slug:"ivan-galtier",fullName:"Iván Galtier"},{id:"183145",title:"Dr.",name:"Antonieta",surname:"Nieto",slug:"antonieta-nieto",fullName:"Antonieta Nieto"},{id:"183146",title:"Dr.",name:"José",surname:"Barroso",slug:"jose-barroso",fullName:"José Barroso"}],corrections:null},{id:"50693",title:"Brain Network Metabolic Changes in Patients with Parkinsonian Tremors",doi:"10.5772/63159",slug:"brain-network-metabolic-changes-in-patients-with-parkinsonian-tremors",totalDownloads:1426,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Functional neuroimaging and modern multivariate analysis techniques have greatly contributed to research into the pathophysiology, diagnosis, and new treatments of neurodegenerative diseases, such as Parkinson’s disease (PD). The pathogenesis of PD symptoms, especially akinesia and rigidity, is associated with abnormalities of cortico-striato-pallido-thalamocortical circuits. Although a resting tremor is one of the cardinal features of PD, the pathophysiology underlying this symptom is unclear and is thought to differ from those of akinesia and rigidity. The application of network analyses to metabolic positron emission tomography scans of patients with PD has provided valuable information concerning functional neural connectivity and identified the patterns of covariance that are specific to the motor manifestations and many nonmotor features of the disease, such as cognitive dysfunction. Functional imaging methods have revealed PD-specific brain activation patterns, including a parkinsonian tremor-related network. Network-based algorithms might aid in the clinical diagnosis of patients with PD from early symptoms and provide objective evidence of treatment responses.",signatures:"Hideo Mure, David Eidelberg and Satoshi Goto",downloadPdfUrl:"/chapter/pdf-download/50693",previewPdfUrl:"/chapter/pdf-preview/50693",authors:[{id:"181695",title:"Prof.",name:"Satoshi",surname:"Goto",slug:"satoshi-goto",fullName:"Satoshi Goto"},{id:"183340",title:"Dr.",name:"David",surname:"Eidelberg",slug:"david-eidelberg",fullName:"David Eidelberg"},{id:"183341",title:"Dr.",name:"Hideo",surname:"Mure",slug:"hideo-mure",fullName:"Hideo Mure"}],corrections:null},{id:"51004",title:"Animal Models of Parkinson’s Disease",doi:"10.5772/63328",slug:"animal-models-of-parkinson-s-disease",totalDownloads:4100,totalCrossrefCites:5,totalDimensionsCites:6,hasAltmetrics:0,abstract:"Parkinson's disease (PD) is a neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta, the consequent dopamine deficit in the striatum and the accumulation of aggregated α‐synuclein (α‐syn) in specific brain regions. The underlying pathophysiology of PD remains poorly understood. Animal models are the best tools to study the pathogenesis of PD. Most studies in PD animal models have focused on the motor features associated with dopamine depletion but still the molecular basis of PD and the molecular pathways of cell death remain unknown. While cellular models have helped to identify specific events, in vivo animal models have simulated most, although not all, of the hallmarks of PD and are useful for testing new neuroprotective approaches. In this chapter, we provide a summary of the most used PD animal models, including their advantages and limitations. Classically, in vivo PD animal models can be divided into those using environmental or synthetic neurotoxins (toxin‐based models) or those utilizing the in vivo expression of PD‐related mutations (genetic models). These models include 6‐hydroxydopamine (6‐OHDA), 1‐methyl‐1,2,3,6‐tetrahydropyridine (MPTP), rotenone, and paraquat, as well as genetic models such as those related to α‐syn, PINK1, Parkin, DJ‐1, and LRRK2.",signatures:"Javier Blesa, Ines Trigo‐Damas, Ana Quiroga‐Varela and Natalia\nLopez‐Gonzalez del Rey",downloadPdfUrl:"/chapter/pdf-download/51004",previewPdfUrl:"/chapter/pdf-preview/51004",authors:[{id:"182798",title:"Dr.",name:"Javier",surname:"Blesa",slug:"javier-blesa",fullName:"Javier Blesa"},{id:"186767",title:"Dr.",name:"Ines",surname:"Trigo-Damas",slug:"ines-trigo-damas",fullName:"Ines Trigo-Damas"},{id:"186768",title:"Dr.",name:"Ana",surname:"Quiroga-Varela",slug:"ana-quiroga-varela",fullName:"Ana Quiroga-Varela"},{id:"186769",title:"MSc.",name:"Natalia",surname:"Lopez-Gonzalez Del Rey",slug:"natalia-lopez-gonzalez-del-rey",fullName:"Natalia Lopez-Gonzalez Del Rey"},{id:"186770",title:"Dr.",name:"Jose A.",surname:"Obeso",slug:"jose-a.-obeso",fullName:"Jose A. Obeso"}],corrections:null},{id:"50961",title:"Understanding Pathophysiology of Sporadic Parkinson's Disease in Drosophila Model: Potential Opportunities and Notable Limitations",doi:"10.5772/63767",slug:"understanding-pathophysiology-of-sporadic-parkinson-s-disease-in-drosophila-model-potential-opportun",totalDownloads:1398,totalCrossrefCites:3,totalDimensionsCites:4,hasAltmetrics:0,abstract:"Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population over age 50. PD is widely accepted as a multifactorial disease with both genetic and environmental contributions. Despite extensive research conducted in the area the precise etiological factors responsible remain elusive. In about 95% Parkinsonism is considered to have a sporadic component. There are currently no established curative, preventative, or disease-modifying interventions, stemming from a poor understanding of the molecular mechanisms of pathogenesis. Here lies the importance of animal models. Pharmacological insults cause Parkinsonian like phenotypes in Drosophila, thereby modelling sporadic PD. The pesticides paraquat and rotenone induced oxidative damage causing cluster specific DA neuron loss together with motor deficits. Studies in fly PD model have deciphered that signaling pathways such as phosphatidylinositol 3-kinase (PI3K/Akt and target of rapamycin (TOR), c-Jun N-terminal kinase (JNK) have been defective. Further, these studies have demonstrated that fruit fly can be a potential model to screen chemical compounds for their neuroprotective efficacy.",signatures:"Priyanka Modi, Ayajuddin Mohamad, Limamanen Phom, Zevelou\nKoza, Abhik Das, Rahul Chaurasia, Saikat Samadder, Bovito Achumi, Muralidhara, Rajesh Singh Pukhrambam and Sarat Chandra\nYenisetti",downloadPdfUrl:"/chapter/pdf-download/50961",previewPdfUrl:"/chapter/pdf-preview/50961",authors:[{id:"181774",title:"Prof.",name:"Sarat Chandra",surname:"Yenisetti",slug:"sarat-chandra-yenisetti",fullName:"Sarat Chandra Yenisetti"},{id:"192493",title:"Dr.",name:"Priyanka",surname:"Modi",slug:"priyanka-modi",fullName:"Priyanka Modi"},{id:"192494",title:"Mr.",name:"Ayajuddin",surname:"Mohamad",slug:"ayajuddin-mohamad",fullName:"Ayajuddin Mohamad"},{id:"192496",title:"Dr.",name:"Limamanen",surname:"Phom",slug:"limamanen-phom",fullName:"Limamanen Phom"},{id:"192499",title:"Dr.",name:"Zevelou",surname:"Koza",slug:"zevelou-koza",fullName:"Zevelou Koza"},{id:"192500",title:"Dr.",name:"Abhik",surname:"Das",slug:"abhik-das",fullName:"Abhik Das"},{id:"192501",title:"Dr.",name:"Rahul",surname:"Chaurasia",slug:"rahul-chaurasia",fullName:"Rahul Chaurasia"},{id:"192502",title:"Dr.",name:"Saikat",surname:"Samadder",slug:"saikat-samadder",fullName:"Saikat Samadder"},{id:"192503",title:"Dr.",name:"Bovito",surname:"Achumi",slug:"bovito-achumi",fullName:"Bovito Achumi"},{id:"192508",title:"Dr.",name:"Rajesh Singh",surname:"Pukhrambam",slug:"rajesh-singh-pukhrambam",fullName:"Rajesh Singh Pukhrambam"},{id:"192509",title:"Dr.",name:null,surname:"Muralidhara",slug:"muralidhara",fullName:"Muralidhara"}],corrections:null},{id:"50238",title:"Pharmacotherapeutic Challenges in Parkinson’s Disease Inpatients",doi:"10.5772/62561",slug:"pharmacotherapeutic-challenges-in-parkinson-s-disease-inpatients",totalDownloads:1712,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"During the natural history of Parkinson’s disease (PD), many patients require hospital admission for medical or surgical problems other than the motor features of PD. Therefore, they are often admitted to non-neurological wards where the staff is unfamiliar with PD management. Among the issues related to hospitalization in patients with PD, drug-related problems such as inappropriate levodopa timing of administration, the use of contraindicated, centrally acting antidopaminergic drugs and anticholinergic burden remain among the most troublesome.",signatures:"Unax Lertxundi, Rafael Hernández, Saioa Domingo-Echaburu, Javier\nPeral-Aguirregoitia and Juan Medrano",downloadPdfUrl:"/chapter/pdf-download/50238",previewPdfUrl:"/chapter/pdf-preview/50238",authors:[{id:"183172",title:"Mr.",name:"Unax",surname:"Lertxundi",slug:"unax-lertxundi",fullName:"Unax Lertxundi"},{id:"185354",title:"Dr.",name:"Rafael",surname:"Hernández",slug:"rafael-hernandez",fullName:"Rafael Hernández"},{id:"185355",title:"Mrs.",name:"Saioa",surname:"Domingo-Echaburu",slug:"saioa-domingo-echaburu",fullName:"Saioa Domingo-Echaburu"},{id:"185356",title:"Mr.",name:"Javier",surname:"Peral-Aguirregoitia",slug:"javier-peral-aguirregoitia",fullName:"Javier Peral-Aguirregoitia"},{id:"185357",title:"Dr.",name:"Juan",surname:"Medrano",slug:"juan-medrano",fullName:"Juan Medrano"}],corrections:null},{id:"50853",title:"Clinical and Experimental Cell Therapy in Parkinson’s Disease",doi:"10.5772/63764",slug:"clinical-and-experimental-cell-therapy-in-parkinson-s-disease",totalDownloads:1242,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Parkinson’s disease (PD), a chronic neurodegenerative disorder, is characterized as a movement disorder with resting tremor, dyskinesia, gait disturbance, etc. The main pathology is based on the progressive loss of dopaminergic neurons in the substantia nigra of the midbrain. These motor symptoms can be treated by dopaminergic drugs, but over time, the drug’s effect has less efficacy, and side effects develop such as involuntary movements. As there is no gold standard long-term treatment for this condition, there is a strong need to develop new drugs and therapies. The clinical and experimental findings of successful intrastriatal transplantation of fetal mesencephalic dopaminergic neurons into the brains of patients with PD have been well established. The development of human stem cell technology including embryonic stem (ES) cells or induced pluripotent stem (iPS) cells opened a new field called clinical cell therapy, especially for PD. In this chapter, we cover the scientific progress of the clinical and experimental trials of cell therapy for patients with PD. It also contains the recent advances in the clinical application of stem cells including neural stem cells, mesencephalic stem cell, ESC, and iPS cells and unsolved problems in the clinical setting. The combination of gene therapy and gene-manipulated stem cell application in PD therapy will be the most discussed in this area.",signatures:"Keun-A Chang and Seonghan Kim",downloadPdfUrl:"/chapter/pdf-download/50853",previewPdfUrl:"/chapter/pdf-preview/50853",authors:[{id:"183327",title:"Prof.",name:"Keun-A",surname:"Chang",slug:"keun-a-chang",fullName:"Keun-A Chang"},{id:"189275",title:"Prof.",name:"Seonghan",surname:"Kim",slug:"seonghan-kim",fullName:"Seonghan Kim"}],corrections:null},{id:"50893",title:"Cell-Based Therapies for Parkinson’s Disease: Preclinical and Clinical Perspectives",doi:"10.5772/63747",slug:"cell-based-therapies-for-parkinson-s-disease-preclinical-and-clinical-perspectives",totalDownloads:1389,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Parkinson’s Disease (PD) is a highly prevalent neurodegenerative disease that affects millions of people globally and remains without definitive treatment. There have been many recent advances in cell-based therapy to replace lost neural circuitry and provide chronic biological sources of therapeutic agents to disease-affected brain regions. Early neural transplantation studies highlighted the challenges of immune rejection, graft integration, and the need for renewable, autologous graft sources. Neurotrophic factors (NTFs) offer a potential class of cytoprotective agents that may complement dopamine (DA) replacement and cell-based therapies in PD. In fact, chronic NTF delivery may be an integral goal of cell transplantation in PD, with ideal grafts consisting of autologous drug (e.g., DA, NTF)-producing cells capable of integration and function in the host brain. This chapter outlines the past and recent preclinical and clinical advances in cell-based and NTF therapies as promising and integrated approaches for the treatment of PD.",signatures:"Andrea R. Di Sebastiano, Michael D. Staudt, Simon M. Benoit, Hu\nXu, Matthew O. Hebb and Susanne Schmid",downloadPdfUrl:"/chapter/pdf-download/50893",previewPdfUrl:"/chapter/pdf-preview/50893",authors:[{id:"183532",title:"Dr.",name:"Susanne",surname:"Schmid",slug:"susanne-schmid",fullName:"Susanne Schmid"},{id:"186621",title:"Dr.",name:"Andrea R.",surname:"DiSebastiano",slug:"andrea-r.-disebastiano",fullName:"Andrea R. DiSebastiano"},{id:"186623",title:"Dr.",name:"Michael",surname:"Staudt",slug:"michael-staudt",fullName:"Michael Staudt"},{id:"186624",title:"Dr.",name:"Matthew O.",surname:"Hebb",slug:"matthew-o.-hebb",fullName:"Matthew O. Hebb"},{id:"186625",title:"Dr.",name:"Hu",surname:"Xu",slug:"hu-xu",fullName:"Hu Xu"},{id:"186626",title:"Mr.",name:"Simon",surname:"Benoit",slug:"simon-benoit",fullName:"Simon Benoit"}],corrections:null},{id:"51310",title:"Stem Cell Therapy for Parkinson's Disease",doi:"10.5772/63340",slug:"stem-cell-therapy-for-parkinson-s-disease",totalDownloads:1669,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Parkinson's disease (PD) is the second most common neurodegenerative disorder of aging after Alzheimer's disease (AD). Pathologically, it is characterized by a degeneration of dopamine (DA) neurons in substantia nigra of middle brain, which causes the motor symptoms and nonmotor symptoms of PD. The dopamine replacement therapy using levodopa and surgical treatment of deep brain stimulation (DBS) can only improve the symptoms of PD, but cannot stop the disease progression. Because of the selective loss of DA neurons, cell transplantation provides an exciting potential for the treatment of Parkinson's disease. The available cell sources include mesenchymal stem cells (MSCs) from bone marrow, neural stem cells (NSCs) from fetal brain tissues, embryonic stem cells (ESCs) from blastocysts, and induced pluripotent stem cells (iPSCs) reprogrammed from somatic cells transfected with stem cell transcription factors of OCT4, SOX2, KLF4, and c‐MYC. Here, we first review the research advance conducted in animal models and patients of PD with these cells, then moving forward to recent development of iPSCs as a future source for the treatment of PD, and highlight the current challenges to make good manufacturing practice (GMP) standard cells suitable for large‐scale production to move the cell‐based therapy from dish to clinic as soon as possible.",signatures:"Fabin Han",downloadPdfUrl:"/chapter/pdf-download/51310",previewPdfUrl:"/chapter/pdf-preview/51310",authors:[{id:"181160",title:"Prof.",name:"Fabin",surname:"Han",slug:"fabin-han",fullName:"Fabin Han"}],corrections:null},{id:"50429",title:"Surgical Therapy of Parkinson's Disease",doi:"10.5772/62884",slug:"surgical-therapy-of-parkinson-s-disease",totalDownloads:1453,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"The history of surgical treatment of Parkinson's disease (PD) covers more than 100 years. It started from lesional approach and evolved to the final deep brain stimulation (DBS) only in the 1990s. The aim of this treatment was to reduce clinical manifestation of PD and drug intake by acting directly on the altered motor pathways. The typical targets are represented by ventralis intermedius thalamic nucleus (VIM), internal globus pallidus nucleus (GPi), and subthalamic nucleus (STN) with more recent extension on other anatomical structures as pedunculopontine nucleus (PPN). Patients are selected according to CAPSIT protocol and undergo DBS when medical treatment has failed to effectively control the symptoms. Clinical benefits are represented by the reduction of “off” time and “on” time with dyskinesia. However, even DBS treatment is characterized by complications and side effects, as intracerebral hemorrhages, infections, ischemia, and seizures. The recent introduction of neuronavigation systems and the amelioration in neuroradiological imaging quality simplified preoperative DBS planning and consequently reduced surgical‐related problems",signatures:"Massimo Piacentino, Giacomo Beggio and Lorenzo Volpin",downloadPdfUrl:"/chapter/pdf-download/50429",previewPdfUrl:"/chapter/pdf-preview/50429",authors:[{id:"181681",title:"Dr.",name:"Massimo",surname:"Piacentino",slug:"massimo-piacentino",fullName:"Massimo Piacentino"},{id:"186117",title:"Dr.",name:"Giacomo",surname:"Beggio",slug:"giacomo-beggio",fullName:"Giacomo Beggio"},{id:"186118",title:"Dr.",name:"Lorenzo",surname:"Volpin",slug:"lorenzo-volpin",fullName:"Lorenzo Volpin"}],corrections:null},{id:"50468",title:"Neuro-Ophthalmologic Evaluation as a Biomarker for Diagnosis and Progression in Parkinson Disease",doi:"10.5772/62877",slug:"neuro-ophthalmologic-evaluation-as-a-biomarker-for-diagnosis-and-progression-in-parkinson-disease",totalDownloads:1563,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Objectives: The purpose of current neuro-ophthalmologic research is to evaluate visual dysfunction and its correlation with structural changes in the retina of patients with Parkinson’s disease and to examine whether there is an association between retinal thinning and disease progression.",signatures:"María Satue, Vicente Polo, Sofía Otin, Jose M. Larrosa, Javier Obis and Elena Garcia-Martin",downloadPdfUrl:"/chapter/pdf-download/50468",previewPdfUrl:"/chapter/pdf-preview/50468",authors:[{id:"182192",title:"Dr.",name:"Maria",surname:"Satue",slug:"maria-satue",fullName:"Maria Satue"},{id:"182717",title:"Dr.",name:"Vicente",surname:"Polo",slug:"vicente-polo",fullName:"Vicente Polo"},{id:"182718",title:"Dr.",name:"Sofia",surname:"Otin",slug:"sofia-otin",fullName:"Sofia Otin"},{id:"182719",title:"Dr.",name:"Jose M.",surname:"Larrosa",slug:"jose-m.-larrosa",fullName:"Jose M. Larrosa"},{id:"182720",title:"Prof.",name:"Luis E.",surname:"Pablo",slug:"luis-e.-pablo",fullName:"Luis E. Pablo"},{id:"182721",title:"Dr.",name:"Elena",surname:"Garcia-Martin",slug:"elena-garcia-martin",fullName:"Elena Garcia-Martin"},{id:"186145",title:"Dr.",name:"Javier",surname:"Obis",slug:"javier-obis",fullName:"Javier Obis"}],corrections:null},{id:"51287",title:"Possible Treatments of Atypical Parkinsonism",doi:"10.5772/63948",slug:"possible-treatments-of-atypical-parkinsonism",totalDownloads:1617,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Success in treating patients with atypical parkinsonism remains exceedingly low. It is particularly important for both neurologists and general practitioners to have a guideline in the actual possible cure options. This study reviews the limited available literature reporting treatment trials about treatment in parkinsonism. Various therapeutical approaches have been tried with rasagiline, immunoglobulin, autologous mesenchymal stem cells, davunetide, lithium, and tideglusib. Recently, transdermal rotigotine (RTG) has been proposed for the treatment of atypical parkinsonism, as well as deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) alone or combined with globus pallidus internus (Gpi) stimulation. The outcomes reviewed here highlight the need for the development of randomized, placebo-controlled trials to validate outcomes about rotigotine, DBS, and all other new therapies directed at altering the underlying biological mechanisms involved in the disease process.",signatures:"Moretti Davide Vito",downloadPdfUrl:"/chapter/pdf-download/51287",previewPdfUrl:"/chapter/pdf-preview/51287",authors:[{id:"147154",title:"Dr.",name:"Davide",surname:"Moretti",slug:"davide-moretti",fullName:"Davide Moretti"}],corrections:null},{id:"51054",title:"The Role of Nurses in Parkinson's Disease",doi:"10.5772/63162",slug:"the-role-of-nurses-in-parkinson-s-disease",totalDownloads:5358,totalCrossrefCites:2,totalDimensionsCites:2,hasAltmetrics:1,abstract:"Background: The complexity of motor and nonmotor symptoms in patients with Parkinson's disease (PD) requires multidisciplinary health actions.",signatures:"Michelle Hyczy de Siqueira Tosin and Beatriz Guitton Renaud\nBaptista de Oliveira",downloadPdfUrl:"/chapter/pdf-download/51054",previewPdfUrl:"/chapter/pdf-preview/51054",authors:[{id:"181642",title:"Dr.",name:"Michelle",surname:"Tosin",slug:"michelle-tosin",fullName:"Michelle Tosin"},{id:"182956",title:"Prof.",name:"Beatriz",surname:"Oliveira",slug:"beatriz-oliveira",fullName:"Beatriz Oliveira"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"5806",title:"Senescence",subtitle:"Physiology or Pathology",isOpenForSubmission:!1,hash:"a8b68766b3057a8d6b4d30695e00f576",slug:"senescence-physiology-or-pathology",bookSignature:"Jolanta Dorszewska and Wojciech Kozubski",coverURL:"https://cdn.intechopen.com/books/images_new/5806.jpg",editedByType:"Edited by",editors:[{id:"31962",title:"Dr.",name:"Jolanta",surname:"Dorszewska",slug:"jolanta-dorszewska",fullName:"Jolanta Dorszewska"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6614",title:"Alzheimer's Disease",subtitle:"The 21st Century Challenge",isOpenForSubmission:!1,hash:"91df6c15517737c8fb91543f870d484d",slug:"alzheimer-s-disease-the-21st-century-challenge",bookSignature:"Jolanta Dorszewska and Wojciech Kozubski",coverURL:"https://cdn.intechopen.com/books/images_new/6614.jpg",editedByType:"Edited by",editors:[{id:"31962",title:"Dr.",name:"Jolanta",surname:"Dorszewska",slug:"jolanta-dorszewska",fullName:"Jolanta Dorszewska"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1191",title:"Neuromuscular Disorders",subtitle:null,isOpenForSubmission:!1,hash:"6f634511340dcd5fe321e13e83a62531",slug:"neuromuscular-disorders",bookSignature:"Ashraf Zaher",coverURL:"https://cdn.intechopen.com/books/images_new/1191.jpg",editedByType:"Edited by",editors:[{id:"66392",title:"Prof.",name:"Ashraf",surname:"Zaher",slug:"ashraf-zaher",fullName:"Ashraf Zaher"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"745",title:"Neurodegenerative Diseases",subtitle:"Processes, Prevention, Protection and Monitoring",isOpenForSubmission:!1,hash:"3d5795dad33257368f0b7848c22d5dd4",slug:"neurodegenerative-diseases-processes-prevention-protection-and-monitoring",bookSignature:"Raymond Chuen-Chung Chang",coverURL:"https://cdn.intechopen.com/books/images_new/745.jpg",editedByType:"Edited by",editors:[{id:"33396",title:"Dr.",name:"Raymond Chuen-Chung",surname:"Chang",slug:"raymond-chuen-chung-chang",fullName:"Raymond Chuen-Chung Chang"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3278",title:"Neurodegenerative Diseases",subtitle:null,isOpenForSubmission:!1,hash:"aa717c2801cf98db641d48414cef8ced",slug:"neurodegenerative-diseases",bookSignature:"Uday Kishore",coverURL:"https://cdn.intechopen.com/books/images_new/3278.jpg",editedByType:"Edited by",editors:[{id:"155691",title:"Dr.",name:"Uday",surname:"Kishore",slug:"uday-kishore",fullName:"Uday Kishore"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"434",title:"Alzheimer's Disease Pathogenesis",subtitle:"Core Concepts, Shifting Paradigms and Therapeutic Targets",isOpenForSubmission:!1,hash:"49f4c7dbf69e8a9eaf780e37f4aae1ab",slug:"alzheimer-s-disease-pathogenesis-core-concepts-shifting-paradigms-and-therapeutic-targets",bookSignature:"Suzanne De La Monte",coverURL:"https://cdn.intechopen.com/books/images_new/434.jpg",editedByType:"Edited by",editors:[{id:"29111",title:"Dr.",name:"Suzanne",surname:"De La Monte",slug:"suzanne-de-la-monte",fullName:"Suzanne De La Monte"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3296",title:"Understanding Alzheimer's Disease",subtitle:null,isOpenForSubmission:!1,hash:"b040d696d429a2a6dc90cd236f160778",slug:"understanding-alzheimer-s-disease",bookSignature:"Inga Zerr",coverURL:"https://cdn.intechopen.com/books/images_new/3296.jpg",editedByType:"Edited by",editors:[{id:"26013",title:"Prof.",name:"Inga",surname:"Zerr",slug:"inga-zerr",fullName:"Inga Zerr"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3437",title:"Mood Disorders",subtitle:null,isOpenForSubmission:!1,hash:"62c54b70da87ce48e712c07601105311",slug:"mood-disorders",bookSignature:"Nese Kocabasoglu",coverURL:"https://cdn.intechopen.com/books/images_new/3437.jpg",editedByType:"Edited by",editors:[{id:"91417",title:"Prof.",name:"Nese",surname:"Kocabasoglu",slug:"nese-kocabasoglu",fullName:"Nese Kocabasoglu"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1062",title:"Dystonia",subtitle:"The Many Facets",isOpenForSubmission:!1,hash:"81069e5ab5b7c4bb52cf7bd16d0c4cb2",slug:"dystonia-the-many-facets",bookSignature:"Raymond L. Rosales",coverURL:"https://cdn.intechopen.com/books/images_new/1062.jpg",editedByType:"Edited by",editors:[{id:"70147",title:"Prof.",name:"Raymond",surname:"Rosales",slug:"raymond-rosales",fullName:"Raymond Rosales"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1360",title:"Mechanisms in Parkinson's Disease",subtitle:"Models and Treatments",isOpenForSubmission:!1,hash:"823c4dc5acbf952ba3723cae01f7f67a",slug:"mechanisms-in-parkinson-s-disease-models-and-treatments",bookSignature:"Juliana Dushanova",coverURL:"https://cdn.intechopen.com/books/images_new/1360.jpg",editedByType:"Edited by",editors:[{id:"36845",title:"Dr.",name:"Juliana",surname:"Dushanova",slug:"juliana-dushanova",fullName:"Juliana Dushanova"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],ofsBooks:[]},correction:{item:{id:"72959",slug:"erratum-driving-control-technologies-of-new-high-efficient-motors",title:"Erratum - Driving Control Technologies of New High-Efficient Motors",doi:null,correctionPDFUrl:"https://cdn.intechopen.com/pdfs/72959.pdf",downloadPdfUrl:"/chapter/pdf-download/72959",previewPdfUrl:"/chapter/pdf-preview/72959",totalDownloads:null,totalCrossrefCites:null,bibtexUrl:"/chapter/bibtex/72959",risUrl:"/chapter/ris/72959",chapter:{id:"68411",slug:"driving-control-technologies-of-new-high-efficient-motors",signatures:"Chang-Ming Liaw, Min-Ze Lu, Ping-Hong Jhou and Kuan-Yu Chou",dateSubmitted:"April 1st 2019",dateReviewed:"July 2nd 2019",datePrePublished:"August 22nd 2019",datePublished:"March 25th 2020",book:{id:"9290",title:"Applied Electromechanical Devices and Machines for Electric Mobility Solutions",subtitle:null,fullTitle:"Applied Electromechanical Devices and Machines for Electric Mobility Solutions",slug:"applied-electromechanical-devices-and-machines-for-electric-mobility-solutions",publishedDate:"March 25th 2020",bookSignature:"Adel El-Shahat and Mircea Ruba",coverURL:"https://cdn.intechopen.com/books/images_new/9290.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"193331",title:"Dr.",name:"Adel",middleName:null,surname:"El-Shahat",slug:"adel-el-shahat",fullName:"Adel El-Shahat"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"37616",title:"Prof.",name:"Chang-Ming",middleName:null,surname:"Liaw",fullName:"Chang-Ming Liaw",slug:"chang-ming-liaw",email:"cmliaw@ee.nthu.edu.tw",position:null,institution:null},{id:"180324",title:"Dr.",name:"Kai-Wei",middleName:null,surname:"Hu",fullName:"Kai-Wei Hu",slug:"kai-wei-hu",email:"kaiweihu@hotmail.com.tw",position:null,institution:{name:"National Tsing Hua University",institutionURL:null,country:{name:"Taiwan"}}},{id:"308019",title:"MSc.",name:"Jia-Hsiang",middleName:null,surname:"Zhuang",fullName:"Jia-Hsiang Zhuang",slug:"jia-hsiang-zhuang",email:"abc0929352983@yahoo.com.tw",position:null,institution:{name:"National Tsing Hua University",institutionURL:null,country:{name:"Taiwan"}}},{id:"308021",title:"MSc.",name:"Shih-Wei",middleName:null,surname:"Su",fullName:"Shih-Wei Su",slug:"shih-wei-su",email:"nthu18356743@gmail.com",position:null,institution:{name:"National Tsing Hua University",institutionURL:null,country:{name:"Taiwan"}}}]}},chapter:{id:"68411",slug:"driving-control-technologies-of-new-high-efficient-motors",signatures:"Chang-Ming Liaw, Min-Ze Lu, Ping-Hong Jhou and Kuan-Yu Chou",dateSubmitted:"April 1st 2019",dateReviewed:"July 2nd 2019",datePrePublished:"August 22nd 2019",datePublished:"March 25th 2020",book:{id:"9290",title:"Applied Electromechanical Devices and Machines for Electric Mobility 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The term ‘Elderly’ is applied to those individuals belonging to age 60 years and above, who represent the fastest growing segment of populations throughout the world. The percentage of elderly in developing countries tends to be small, although numbers are often large. In the year 1990, there were more than 280 million people belonging to the age 60 years or over in developing regions of the world, and 58% of the world’s elderly were living in less-developed regions [1].
According to World Population Prospects (1950–2050), the proportion of elderly in developing countries is rising more rapidly, in comparison with developed ones [2]. The report published by the US Department of Health and Human Services shows that more developed nations have had decades to adjust to this change in age structure (Figures 1 and 2). As we see in Figure 1, it has taken more than a century for France’s population aged 65 or older to rise from 7 to 14%, whereas many developing countries are growing rapidly in number and percentage of older individuals [2].
Speed of population ageing in developed countries. Source: U.S. Census Bureau [
Speed of population ageing in developing countries. Source: U.S. Census Bureau [
It is expected that by the year 2020, 70% of the world’s elderly population will be in developing countries, with the absolute number exceeding 470 million which is double the number of the developed world [5]. The main factor responsible for this changing pattern of population ageing includes a rapid decline in both fertility and premature mortality [6]. Decline in fertility is particularly apparent in some developing countries like China, Cuba and Uruguay, although the fertility level in other developing countries such as Kenya, Zaire and Bangladesh remains high [7].
Ageing is associated with many neurological disorders, as the capacity of the brain to transmit signals and communicate reduces. Loss of brain function is the biggest fear among elderly which includes loss of the very persona from dementia (usually Alzheimer’s disease). Multiple other neurodegenerative conditions like Parkinson’s disease or the sudden devastation of a stroke are also increasingly common with age [8].
Alzheimer’s and Parkinson’s diseases are the progressive neurodegenerative diseases associated with ageing [9]. Alzheimer’s is characterised by progressive cognitive deterioration along with a change in behaviour and a decline in activities of daily living. Alzheimer’s is the most common type of pre-senile and senile dementia. This disease causes nerve cell death and tissue loss throughout the brain, affecting nearly all its functions. The cortex in the brain shrivels up and this damages the areas involved in thinking, planning and remembering. The shrinkage in a nerve cell is especially severe in the hippocampus (an area of the cortex that plays a key role in the formation of new memories) as well as the ventricles (fluid-filled spaces within the brain) also grow larger. Alzheimer’s disease causes an overall misbalance among the elderly by causing memory loss, changes in personality and behaviour-like depression, apathy, social withdrawal, mood swings, distrust in others, irritability and aggressiveness [10, 11].
Nearly, 33 million Indians have neurological disorders, and these occur twice as often in rural areas [12]. According to the World Health Organisation (WHO) [13], nearly 5% of men and 6% of women aged 60 years or above are affected with Alzheimer’s-type dementia worldwide. In India, the total prevalence of dementia per 1000 elderly is 33.6%, of which vascular dementia constitutes approximately 39% and Alzheimer’s disease constitutes approximately 54% [14].
Stroke is another common cause of mortality worldwide [13]. However, in India, the prevalence rate of stroke among elderly is reported to be very low compared to Western countries [15, 16, 17].
A mild decline in the overall accuracy is observed with the beginning of the 60s that progresses slowly, but sustained attention is good in healthy older adults. Cognitive function declines and impairments are frequently observed among the elderly. Normally, these changes occur as outcomes of distal or proximal life events, where distal events are early life experiences such as cultural, physical and social conditions that influence functioning and cognitive development [17].
Cognition decline results from proximal factors (multiple serial cognitive processes) including processing speed, size of working memory, inhibition of extraneous environmental stimuli and sensory losses. This is a threat to the quality of life of those affected individuals and their caregivers [18].
Impaired cognition among elderly is associated with an increased risk of injuries to self or others, the decline in functional activities of daily living and an increased risk of mortality [19, 20, 21]. Mild cognitive impairment is increasingly being recognised as a transitional state between normal ageing and dementia [22, 23].
According to various studies [24, 25, 26], the effect of normal ageing on memory may result from the subtly changing environment within the brain. The brain’s volume peaks at the early 20s and it declines gradually for rest of the life. In the 40s, the cortex starts to shrink and people start noticing the subtle changes in their ability to remember or to do more than one task at a time. Other key areas like neurons shrink or undergo atrophy and a large reduction in the extensiveness of connections among neurons (dendritic loss) is also noticed. During normal ageing, blood flow in the brain decreases and gets less efficient at recruiting different areas into operations. The whole group of changes taking place in the brain with ageing decreases the efficiency of cell-to-cell communication, which declines the ability to retrieve and learn [27]. It also affects the intelligence, especially fluid intelligence (problem-solving with a novel material requiring complex relations) declines rapidly after adolescence. Perceptual motor skills (timed tasks) decline with age [28].
Ageing includes a decline in accommodation (presbyopia), glare tolerance, adaptation, low-contrast activity, attentional visual fields and colour discrimination. Changes occur in central processing and in the components of the eye. These numerous changes affect reading, balancing and driving [29].
Ageing causes conductive and sensory hearing losses (presbycusis); the loss is primarily high tones, making consonants in speech difficult to discriminate [30].
Losing sense of taste is a common problem among adults [31]. Taste acuity does not diminish but salt detection declines. Perception of sweet is unchanged and bitter is exaggerated. The salivary glands get affected, and the volume and quality of saliva diminish. All changes combine to make eating less interesting [32]. Studies show that the physiological decline in the density of the taste acuity and papillae results in a decline of gustatory function [33]. In fact, studies done on taste dysfunction show that ageing-associated changes in the density of taste acuity may affect taste function differently in different regions of the tongue [34]. Taste perception declines during the normal ageing process. A study done on the healthy elderly shows that after about 70 years of age, taste threshold begins to increase resulting in dysgeusia [34]. Chewing problems associated with loss of teeth and use of dentures also interfere with taste sensation and cause reduction in saliva production [32].
As we get older, our olfactory function declines [35]. Hyposmia (reduced ability to smell and to detect odours) is also observed with normal ageing [36]. The sense of smell reduces with an increase in age, and this affects the ability to discriminate between smells. A decreased sense of smell can lead to significant impairment of the quality of life, including taste disturbance and loss of pleasure from eating with resulting changes in weight and digestion [36].
It has been reported that more than 75% of people over the age of 80 years have evidence of major olfactory impairment. Many long-term studies show the evidence of a decline in olfaction considerably after the seventh decade [37]. Another study found that 62.5% of 80–97-year-olds had olfactory impairments [38]. However, it is widely accepted that taste disorders are far less prevalent than olfactory losses with age [38]. Ageing also causes atrophy of olfactory bulb neurons. Central processing is altered, resulting in a decreased perception and less interest in food [39].
As we age, our sense of touch often declines due to skin changes and reduced blood circulation to touch receptors or to the brain and spinal cord. Minor dietary deficiencies such as the deficiency of thiamine may also be a cause of changes [40]. The sense of touch also includes awareness of vibrations and pain. The skin, muscles, tendons, joints and internal organs have receptors that detect touch, temperature or pain [41].
A decline in the sense of touch affects simple motor skills, hand grip strength and balance. Studies have shown that muscle spindle (sensory receptors within the muscle that primarily detects changes in the length of this muscle) and mechanoreceptor (a sense organ or a cell that responds to mechanical stimuli such as touch or sound) functions decline with ageing, further interfering with balance [42].
Normal ageing is characterised by a decrease in bone and muscle mass and an increase in adiposity [43, 44]. A decline in muscle mass and a reduction in muscle strength lead to risk of fractures, frailty, reduction in the quality of life and loss of independence [45]. These changes in musculoskeletal system reflect the ageing process as well as consequences of a reduced physical activity. The muscle wasting in frail older persons is termed ‘sarcopaenia’. This disorder leads to a higher incidence of falls and fractures and a functional decline. Functional sarcopaenia or age-related musculoskeletal changes affect 7% of elderly above the age of 70 years, and the rate of deterioration increases with time, affecting over 20% of the elderly by the age of 80 [46]. Strength declines at 1.5% per year, and this accelerates to as much as 3% per year after 60 years of age [47]. These rates were considered high in sedentary individuals and twice as high in men as compared with those in women [48]. However, studies show that on an average, men have larger amounts of muscle mass and a shorter survival than women. This makes sarcopaenia potentially a greater public health concern among women than among men [48].
Skeletal muscle strength (force-generating capacity) also gets reduced with ageing [45, 46] depending upon genetic, dietary and, environmental factors as well as lifestyle choices. This reduction in muscle strength causes problems in physical mobility and activity of daily living. The total amount of muscle fibres is decreased due to a depressed productive capacity of cells to produce protein. There is a decrease in the size of muscle cells, fibres and tissues along with the total loss of muscle power, muscle bulk and muscle strength of all major muscle groups like deltoids, biceps, triceps, hamstrings, gastrocnemius (calf muscle), and so on. Wear and tear or wasting of the protective cartilage of joints occurs. The cartilage normally acts as a shock absorber and a gliding agent that prevents the friction injuries of the bone. There are stiffening and fibrosis of connective tissue elements that reduce the range of motion and affect the movements by making them less efficient. As part of the normal cell division process, telomere shortening occurs. DNA is more exposed to chemicals, toxins and waste products produced in the body. This whole process increases the vulnerability of cells.
With ageing, toxins and chemicals build up within the body and tissues. As a whole, this damages the integrity of muscle cells. Physical activity also decreases with age, due to a change in lifestyle. Somehow, the physiological changes of the muscles are aggravated by age-related neurological changes [49]. Most of the muscular activities become less efficient and less responsive with ageing as a result of a decrease in the nervous activity and nerve conduction.
A study was done by Williams et al. [50], who evaluated the muscle samples from both elderly and young adults and suggested that limb muscles are 25–35% shorter and less responsive in elderly healthy individuals when compared to young adults. In addition, the overall fat content of muscles was also higher in elderly population, suggesting transformation in the normal remodelling with age. Age-related musculoskeletal changes are much more prominent in fast-twitch muscle fibres as compared to slow-twitch muscle fibres. With ageing, the total water content of the tissue decreases and loss of hydration also adds to the inelasticity and stiffness. Alterations in the basal metabolic rate and slowing metabolism (as part of the physiological ageing process) result in muscle changes. This leads to the replacement of proteins with fatty tissue (that makes muscle less efficient).
Hormonal disorders can affect the metabolism of bones as well as muscles. Research suggests that menopause in women marks the aggravation in the deterioration of musculoskeletal changes due to lack of oestrogen that is required for the remodelling of bones and soft tissues. Certain systemic conditions like vascular disorders or metabolic disorders, in the case of diabetes, affect the remodelling of tissues as the rate or volume of nutritional delivery for the regeneration of cells is compromised. It is very important to control the pathological processes to optimise healing and repairing the potential of the musculoskeletal system. Essential vitamins like vitamin D and vitamin C play major roles in the functional growth of muscles and bones. Lack of certain minerals like calcium, phosphorus and chromium can be the result of age-related digestive issues. As such, it results in imbalance in the production of certain hormones like calcitonin and parathyroid that regulate the serum concentration of vitamins and minerals (due to tumours that are highly prevalent in elderly) or it causes a decreased absorption from the gut.
Age-related deterioration of muscular strength and balance control mechanisms has been associated with a reduced performance on functional tasks [51, 52, 53]. Comparing the isometric strength levels of the same muscle group, the loss of strength begins sooner among women than among men. It is reported that women are weaker than men in the absolute strength of various muscle groups in all stages of life. Various studies state that women have a longer life span, so the prevalence of disability among women is also more compared with men and it is marked with advancing age [54, 55, 56].
The human body is made up of fat, lean tissue (muscles and organs), bones and water. After the age of 40, people start losing their lean tissue. Body organs like liver, kidneys and other organs start losing some of their cells. This decline in muscle mass is associated with weakness, disability and morbidity [57, 58].
The tendency to become shorter occurs among the different gender groups and in all races. Height loss is associated with ageing changes in the bones, muscles and joints. Studies show that people typically lose almost one-half inch (about 1 cm) every 10 years after age 40 [59]. Height loss is even more rapid after age 70. These changes can be prevented by following a healthy diet, staying physically active and preventing and treating bone loss [60, 61].
Changes in the total body weight vary for men and woman, as men often gain weight until about age 55 and then begin to lose weight later in life. This may be related to a drop in the male sex hormone testosterone. Women usually gain weight until age 67–69 and then begin to lose weight. Weight loss later in life occurs partly because fat replaces lean muscle tissue and fat weighs less than muscle [60]. Studies have also shown that older people may have almost one-third more fat compared to when they were younger. Fat tissue builds up towards the centre of the body, including around the internal organs [60, 62, 63].
Today, as standards of living continue to rise, weight gain is posing a growing threat to the health of inhabitants from countries all over the world. Obesity is a chronic disease, prevalent in both developed and developing countries, and it is affecting all age groups. Indeed, it is now so common that it is replacing the more traditional public health concerns, such as infectious diseases and undernutrition, as the most common and significant contributors of ill health [64, 65, 66, 67] (Figure 3).
Prevalence of obesity among elderly aged 60 years and above, by sex: The United States, 2013. Source: [
As per World Health Organisation (WHO), globally, approximately 2.3 billion elderly people are overweight and more than 700 million elderly people are obese [68]. Most elderly belonging to the middle and high socio-economic groups are prone to obesity and complications related to obesity, due to sedentary lifestyles and a reduced physical mobility [69]. Obesity is considered as one of the major risk factors which causes the onset and increases the severity of non-communicable diseases (NCDs). It is a worldwide health problem, affecting elderly from both developed and developing countries. In elderly, obesity contributes to the early onset of chronic morbidities and functional impairments which lead to premature mortality [70].
The population in developed countries have proportionally a greater number of older adults living to older ages, and the prevalence of obesity is rising progressively, even among this age group [71].
The prevalence of obesity among elderly belonging to United States ranges from 42.5% in women to 38.1% in men, belonging to the age group 60–79 years. The prevalence differs for the elderly belonging to the age group 80 years and above, that is, 19.5% for females and 9.6% for males [72, 73, 74].
Comparatively, the prevalence of obesity in Europe is slightly lower but it is still a significant health issue. The prevalence of obesity among elderly in the United Kingdom is 22% among women and 12% among men aged 75 years or older [70, 75, 76, 77]. These statistics bode ill as the proportion of world’s elderly population is growing rapidly (Figure 4).
Trends in weight by age cohort, 1980–2000 (Australia). Source: Bennett et al. [
In Australia, the percentage of weight gain has been so high that instead of losing weight with an increase in life, men and women aged 60–70 weigh more on average than they did when they were 20 years younger (Figure 5). Australian studies show that the prevalence of obesity among elderly has increased in the age group of 60–69 years at about 24% for males and 30% for females, whereas it is less common among the elderly belonging to age group 80 years and above [78, 80]. Studies show that the percentage of Australian elderly reporting increased abdominal fat is markedly increasing over the years. Based on waist circumference, more than 30% of elderly males and 44% of elderly females in Australia are currently at a substantially increased risk of NCDs [78, 80, 81].
Worldwide prevalence of obesity among elderly women and men with BMI of ≥30 kg/m2. Source: OECD [
Studies from the Netherlands show that obesity was present in 18% of men and 20% of women belonging to the age group of 60 years and above [82]. Also, the increase in waist circumference ranged from 40% among males to 56% among females [82, 83].
In France, studies show that the prevalence of obesity among elderly was relatively stable during early years (1980–1991), 6.4–6.5% in males and 6.3–7.0% among females [83], but studies from recent years [84, 85] have highlighted a sharp increase in obese elderly, 19.5% for both males and females; this prevalence rate decreased gradually after 70 years of age, that is, from 19.5 to 13.2% [86]. The Scottish Health Survey shows that in 10 years (2003–2013), the prevalence of obesity has increased as the body mass index (BMI) continues to rise in people 60–70 years of age, especially among females [87]. In this same period, there was an increased curve shown for the waist circumference (5–10 cm) in both the sexes between 50 and 70 years of age. This inappropriate increase in waist circumference and a slight increase in BMI in the Scottish Health Survey may indicate a substantial gain in visceral fat mass and loss of lean tissue that predisposes to ill health in the obese elderly [88, 89].
In Spain, 35% of subjects aged 65 years or older suffered from obesity (30.6% of males and 38.3% of females) and 61.6% had an increased waist circumference (50.9% of males and 69.7% of females) [88].
Over the past years, obesity among elderly was considered as a problem only in high-income countries, but the trend is changing now; excess weight, as well as obesity, is dramatically increasing in low-income and middle-income countries as well, particularly in urban settings [90]. Various studies show a significant change in the mean body weight, physical activity and diet along with progressive economic development in developing countries. Possibilities are high that obesity and its co-morbidities will continue to affect an increasing number of populations in these regions. Lifestyle and environmental factors are acting in a synergistic manner to fuel the obesity epidemic. As per WHO estimates, there is a decline in undernourished population across the world, whereas the overnourished population has increased to 1.2 billion [90]. A WHO report shows that more than 1 billion elderly are overweight and 300 million are obese. The problem of obesity is increasing in the developing world with more than 115 million people suffering from obesity-related problems [90]. The obesity rate has increased threefold or more since 1980 in the Middle East, the Pacific Islands and India [91, 92]. However, the prevalence of obesity is not as high in all developing countries, like China and some African nations [93].
As per the WHO report, the prevalence of overweight and obese elderly in China was 19.0 and 2.9%, respectively. However, the prevalence has increased over the past years; in the latest study, the prevalence of overweight and obesity among elderly was 21.0 and 7.4% [94, 95]. There was a slight increase in the prevalence of overweight and obesity among women than among men in China.
According to WHO estimates, among all Gulf regions, Kuwait ranked number one with the highest prevalence of overweight and obesity (78.8%) among elderly (60 years and above) [92]. Worldwide, Kuwait is ranked 11th, that is, the highest in obesity among the Arab countries and the Middle East [93, 96]. Studies from Sri Lanka show a prevalence rate of 25.2% for overweight and 9.2% for obesity. The prevalence of central obesity among elderly was highest at 26.2% [97, 98]. The prevalence of overweight and obesity in Brazil was 41.8% for females and 23.4% for males. According to the prevalence studies of obesity among elderly in Nigeria [99], overweight among elderly ranged from 20.3 to 35.1% and obesity ranged from 8.1 to 22.2%. WHO reported that the prevalence of obesity in Sub-Saharan African countries ranged between 3.3 and 18.0% and that obesity has become a leading risk factor for diabetes mellitus and cardiovascular diseases in the urban areas of Africa [93, 99]. The situation can get worse within a decade if the present trend continues and overweight could emerge as the single most important public health problem in adults. Overweight or obesity may not be a specific disease but it is certainly considered as a major contributory factor leading to various degenerative diseases in adult life. Prevention and control of this problem must, therefore, claim priority attention [100].
As per a study done in Delhi on urban elderly, nearly 14% of men and more than 50% of women belonging to what may be a higher-income group (HIG) were overweight (BMI >25) and obese (BMI >30) [101]. The prevalence of abdominal obesity among the elderly group was also reported as high. Assuming that the HIG in India number is around 100 million (half the number of the middle class), it may be computed that there are roughly 40–50 million overweight subjects belonging to the HIG in the country today. Visweswara et al. [102] studied females of Hyderabad (60 years and above) belonging to the high socio-economic status and reported the prevalence rate of obesity as 36.3%. Gopinath et al. [103] studied urban elderly in Delhi and reported the rate of prevalence of obesity as 33.4%. A study done in the Union Territory of Chandigarh showed an increase in BMI (>25) resulting in the high prevalence rate of overweight (33.14%) and obesity (7.54%) among elderly [104, 105].
The relationship between energy intake and energy expenditure is an important determinant of body fat mass. Obesity occurs when the consumption of calories is more than the calorie expenditure. The possible causes of obesity are depicted in Figure 6. Various studies indicate that how much we eat does not decline with advancing age; therefore, it is likely that a decrease in energy expenditure particularly in the beginning of old age (50–65 years) contributes to the increase in body fat as we age [62, 106]. At the age of 65 years and above, hormonal changes cause an accumulation of fat. Ageing is associated with a decline in the secretion of growth hormone, serum testosterone, resistance to leptin and a reduced responsiveness to thyroid hormone [107]. Studies show that resistance to leptin could cause a decrease in the ability to regulate appetite downward [74]. Several other genetic, environmental and social factors contribute to obesity among elderly.
Possible causes of obesity. Source: La Berge [
Science does show a link between obesity and heredity [109]. Various studies indicate that obesity is related to the inherited genes and there is a link between obesity and heredity [110, 111, 112, 113]. According to a study, visceral fat is more influenced by the genotype than subcutaneous fat [114].
Like genetics, environment also has a major role to play in obesity. The food we consume, physical activity and lifestyle behaviour are all influenced by the environment. For example, the adoption of modern diet over traditional diet, the trend towards ‘eating out’ rather than preparing food in the home, the development of high-rise buildings that often lack sidewalks and a deficit of readily accessible recreation areas are some of the common environmental factors associated with obesity.
Poverty and low education level also appeared as a reason for obesity among elderly. Studies state that the lack of nutritional knowledge, purchase of low-cost fat and organ meat are also associated with overweight and obesity. Poor hygienic conditions also appeared as a major reason [114].
Other health issues and illnesses that are associated with obesity and weight gain are hyperthyroidism, polycystic ovary syndrome, Cushing’s syndrome and depression [2]. Obese elderly are more likely to report symptoms of depression, such as hopelessness, sadness or worthlessness [115]. Sleep plays a major role. Lack of sleep contributes to obesity [106]. Certain drugs, such as antidepressants and steroids, may stimulate appetite or cause water retention or reduce the metabolic rate [82], causing an increase in weight. Health issues like arthritis and joint pain decrease mobility and activity intolerance, contributing to obesity [116]. Joint pain decreases mobility, and activity intolerance may lead to weight gain because of a decreased activity. Older adults are more likely than younger adults to experience functional limitations associated with chronic illnesses that may begin a stress-pain-depression cycle that can result in lifestyle patterns leading to obesity [117]. Finally, the complex relationship between lifestyle pattern and functional ability merits attention as a contributor to obesity [93].
In developing countries, as compared to developed countries, gerontology has drawn comparatively lesser attention. This is because the increased life expectancy of elderly resulting in a demographic transition which developing countries are witnessing today has already been faced by developed countries, several decades back. However, in recent years with a rising percentage of elderly population, epidemiologists, researchers, demographers and clinicians have focussed their attention towards elderly care health issues and various problems associated with ageing and numerous implications of this demographic transition.
Elderly face various problems and require a multi-sectoral approach involving inputs from various disciplines of health, psychology, nutrition, sociology and social sciences.
There is no conflict of interest.
In specific, bagasse is scientifically defined as a waste of sugarcane liquid extraction after milling process and is in a fibrous form. Bagasse is one of the biomass resources that is widely used as a boiler fuel in sugar factory, source of animal feed, material of paper, cement and brick reinforcement material [1, 2]. The amount of bagasse production each year is abundant, easily obtained, and economical. Based on the data from Indonesian Sugar Farm Research Center (P3GI) [3], bagasse amounts to approximately 32% of milled sugarcane weight or about 10.2 million ton/year or mill/season all around Indonesia. Furthermore, bagasse contains 48–52% water, sugar (approximately3.3% in average), and fiber at an average of 47.7% [4, 5]. Bagasse fiber is unable to be dissolved in water because mostly it consists of cellulose, pentosane, and lignin [6]. Bagasse waste could be used as a raw material in producing surfactant due to its high lignin content, which is estimated to be approximately 25% [7]. Lignin can be separated from bagasse waste by lignin isolation method and hydrolysis process using sodium hydroxide (NaOH) solution [8, 9]. The process also depends on creating bagasse surface enlargement by minimizing the size of its fiber in order to have the better yields of the isolated product. Lignosulfonate is a derivate of lignin that can be produced by reacting lignin with sodium bisulfite (NaHSO3) at certain reaction conditions via the electrophilic addition reaction [10, 11]. The presence of double bonds within the lignin structure has made lignin to be available for the addition reaction using various electrophilic substances, for instance, the hydrogen sulfite (▬HSO3) group of sodium bisulfite [12]. Thus, the product is categorized as sodium lignosulfonate (SLS) surfactant [13]. In addition, lignosulfonate is one of the variants of anionic surfactant that is often utilized in a chemical injection process of enhanced oil recovery (EOR) in the oil industry [14]. Therefore, the high lignin content in bagasse have made bagasse to be an eligible candidate to produce surfactant and became the aim of this research, which is to produce the lignosulfonate surfactant via sulfonation reaction of lignin previously isolated from bagasse. Based on the observations and search for existing patents, what have been found are patent Nos. 2,837,435 and 4,304,361 regarding the use of bagasse as a raw material for building needs, cutting of bagasse fiber for growing media needs, methods for producing bio-aromatic-based chemicals, bio-based aromatic fuels, and lignin residues [15, 16]. Whereas, the No. 8529731 was found to contain the process of fractionation of bagasse into cellulose, hemicellulose (xylene), and lignin with high-purity α-cellulose, which is a useful raw material for the manufacture of cellulose esters such as cellulose triacetate and cellulose plastics [17]. Amri [18] has shown research on sodium lignosulfonate surfactant which has characteristics of water solubility, hygroscopic, and color properties as well as the polydispersity properties of sample SLS which are generally in accordance with commercial SLS.
The lignin isolation method (hydrolysis) can excite lignin with acid, resulting in acid lignin as shown in Figure 1.
The reaction of lignin and NaOH in the delignification process [
Isolation of lignin is generally carried out using sulfuric acid or hydrochloric acid. Under acidic conditions, the charged lignin will become neutral. Lignin will not dissolve in water and will settle. The resulting solid can be separated by filtering. To change the nature of water-insoluble lignin, lignin can be modified through the sulfonation process to become lignosulfonate [20]. Sulfonation is intended to change the hydrophilic nature of the less polar lignin into a more polar/water-soluble lignosulfonate salt by inserting the sulfonate group and its salt into the lignin hydroxyl group so that the lignosulfonate salt has a structure as a surface-active agent or surfactant [19]. The sulfonate group in the lignosulfonate is a hydrophilic group that causes the lignosulfonate to have an amphipathic structure (surfactant). Figure 2 shows the structure of the lignosulfonate.
Lignosulfonate structure.
The existence of the sulfonate group can be determined by the general formula R-SO3Na which is a simplification of the sulfate R-O-SO3Na [21]. The R group is a group of C8-C22 aromatic carbon atoms which is a hydrophilic group, while the hydrophobic group consists of carboxylates, sulfonates, phosphates, or other organic acids. The sulfonation process is the core process for producing lignosulfonate salts. The reaction occurs between lignin and sulfite salts. There are several types of sulfite salts that can be used in this process, including using sodium bisulfite (NaHSO3) in addition to other ingredients such as Na2SO3, NaOH + CH2 (OH) SO3Na, HCHO + NaOH, C2Cl4 + ClSO3H, or SO32− + CH2O [22].
Several studies on the manufacture of sodium lignosulfonate that have been tried include raw materials for oil palm empty bunches [23], oil palm shells [24], palm frond biomass [18], and bagasse [25, 26]. The results of this study were limited to the manufacture of sodium lignosulfonate products which were correlated with the size of bagasse powder and the concentration of sodium bisulfite. Lignosulfonates, as a result of lignin sulfonation, are currently widely used as emulsifiers in iron ore processing, oil field chemicals, and pesticide formulas [27] as well as dust emission control and stabilizer for the fertilizer industry, animal feed industry, gypsum agent wallboard dispersant, oil well drilling mud additive, brick reinforcement, cement, and mortar [28].
In this study of sulfonation reaction toward lignin isolated from bagasse, this study used bagasse as the main raw material, with chemical reagents being sodium hydroxide, sulfuric acid, sodium bisulfite, and distilled water. Range and specifications are used in the bagasse lignin isolation process consisting of bagasse size 40, 60, and 80 mesh; sodium hydroxide concentration 0.6, 2, 3, 6, 8, and 10 M; and sodium bisulfate concentration 0.25 M. The equipment used in the process of lignin isolation and surfactant sulfonation consists of a sieve shaker; hot plate magnetic stirrer; two- or three-neck flask; condenser; beaker glass 200, 500, and 1000 mL; measuring cup 250 mL; thermometer; rod mixer; burette; gloves; glasses; mask; fume hood; pH meter paper; Buchner funnel; Whatman paper; watch glass; oven; digital balance; 250 and 500 mL reagent bottles; 10-mL vial bottle; and desiccator. The mechanism process of the lignosulfonate surfactant occurs through two reactions, namely, hydrolysis and sulfonation [29]. Hydrolysis is a reaction to break down lignin molecules into smaller molecules so that they can dissolve in water. Sulfonation is a reaction between bisulfite ions and lignin molecules. Previous research results reported that the surfactant methyl ester sulfonate (MES) could be synthesized from the direct sulfonation of palm kernel oil methyl ester using sodium bisulfite solution. The important from this previous research is the sulfuric acid concentration factor which affects the value of the decrease in surface tension, the decrease in interface tension, the stability of the emulsion, and the color of the surfactant [30].
The method of processing bagasse into lignosulfonate is carried out through two processes, namely, the isolation process of lignin from bagasse and the sulfonation process of lignin into sulfonates. The bagasse from the sugar factory was previously sifted coarsely and then to oven to dry completely. Then the oven bagasse is sieved again with a sieve shaker to obtain a particle size of bagasse with a certain mesh, namely, 40 mesh, 60 mesh, 80 mesh, and 100 mesh. Figure 3 shows the bagasse that has been dried and then sieved using a sieve shaker to become a fine powder (Figure 4) [31].
Bagasse.
Mesh of bagasse [
The method used in this study is a development from previous researchers who modified lignosulfonate from lignin. In his research, lignin isolation was carried out using NaOH reaction by heating at a temperature of 60–100°C for 3–10 hours [20]. In this research, the lignin isolation process begins by inserting the bagasse that has been sieved with a sieve shaker into the reaction flask and reflux directly in sodium hydroxide solution at a various concentration for 5 hours at a temperature of 90–100°C. The result of reflux of NaOH is then filtered, diluted, and neutralized by adding dropwise concentrated sulfuric acid (H2SO4) to pH = 2 and allowed to stand for at least 8 hours until a precipitate appears, then filtered, and dried in an oven at 70°C. In this filtering process, it is accompanied by rinsing with distilled water because lignin does not dissolve in water and this rinsing with distilled water will dissolve the remaining glucose that may still be present in the results of the lignin isolation. The precipitate obtained is lignin isolated from bagasse and after drying using a vacuum oven, it becomes a brown powder.
The lignin isolation process starts with 5 gram of dry bagasse powder of each mesh size which is put into a three-neck flask, then NaOH is added until the bagasse is submerged and heated for 5 hours using a hot plate magnetic stirrer at a temperature of 90–100°C. The reflux filtrate which still contains NaOH is taken and diluted with water at a volume ratio of 1:1. The solution is then added dropwise to H2SO until it reaches pH = 2, then this solution is left to stand to get a precipitate for at least 8 hours. The precipitate that is formed is filtered and then dried in an oven. The structure of isolated lignin product was determined through FTIR spectrophotometric measurements which were then compared with the standard lignin FTIR spectrum. In the lignin isolation process, optimization was also carried out using the concentration of NaOH used, namely, with a concentration range of 2, 3, 6, 8, and 10 M. Each NaOH concentration is used in the lignin isolation process by varying the size of the bagasse mesh.
The synthesis of bagasse into sodium lignosulfonate begins with the preparation of bagasse powder which will be isolated to separate the lignin from the bagasse. After lignin is formed, a Fourier transform infrared (FTIR) [32, 33] test must be carried out to ensure the presence of lignin-forming components. The standard lignin used is commercial lignin from the lignin product of Aldrich and Kraft. If the component has not been formed, it must return to the isolation process again with changes to the variables used. There are three components of the main functional groups as indicators of lignin formation, namely, the phenolic O▬H functional groups, the aliphatic and aromatic ▬CH▬ stretching groups, and the C═C aromatic functional groups. In the lignin isolation process, the variables used are NaOH concentration, duration of the isolation process, and temperature in the isolation process. This looping process is carried out continuously until the lignin component is obtained that is in accordance with the existing commercial lignin standards. If the lignin formed meets the component requirements, it can be continued to the sulfonation process. The result of this sulfonation process is a brown powder of sodium lignosulfonate (SLS) surfactant. This product must also perform component characterization using the FTIR test. If the FTIR test results do not show any lignosulfonate-forming components, then a looping process is carried out until the sulfonation process produces a lignosulfonate component that matches the standard lignosulfonate. The standard lignosulfonates used are Patricia and Aldrich standards [34].
The components of the lignosulfonate that must be present include the stretching vibration of the alkene functional group ▬C═C▬aromatic, the stretching vibration of the sulfonate functional group S═O, the bending vibration of the C═O functional group carboxylate group, and the bending vibration of the S-OR ester functional group. At this stage, it can be said that the synthesis process is complete, as illustrated in Figure 5. The process of synthesis of bagasse into sodium lignosulfonate surfactant as a whole can be seen in Figure 5.
Schematic synthesis of bagasse into sodium lignosulfonate [
The sulfonation process is a procedure in the form of adaptation and modification from research conducted by Ari [25] and Furi [26]. A total of 8 gram of isolated bagasse lignin was put into a three-neck flask, then sodium bisulfite solution was added, and then heated (refluxed) at 150°C for 5 hours. The reaction product is cooled and precipitated and further dried in a vacuum oven. From this sulfonation process, it produces a surfactant called sodium lignosulfonate (SLS). The structure of SLS surfactant was determined through FTIR, LCMS, and NMR spectrophotometric measurements [36]. The FTIR test results were then compared with the main components of the commonly used commercial lignosulfonate [34]. If it is in accordance with the components forming the SLS surfactant, this product can be said to have been successfully obtained. If it is not accordance with the standard components that should be present in the lignosulfonate, the sulfonation process is repeated with different parameters.
Furthermore, the lignosulfonate monomer structure test was carried out using gas chromatograph mass spectrum (GCMS) and nuclear magnetic resonance (NMR). The structure of the lignosulfonate monomer is needed in order to help see the suitability of the use of the surfactant lignosulfonate against the crude oil to be injected by the lignosulfonate.
The lignin isolation process has been carried out several times with variations in the concentration of NaOH and the size of the mesh bagasse. Variations in bagasse mesh sizes used were 40 mesh, 60 mesh, 80 mesh, and 100 mesh, and the concentration of NaOH was 2, 3, 6, 8, and 10 M. Figure 6 shows the results of lignin isolation in the form of a dark brown powder.
Lignin from bagasse isolation.
From the experiment as many as 15 variations, only four variations met the requirements, namely, lignin results above 60% and they had lignin-forming components, namely, lignin (80–3), lignin (60–8), lignin (40–10), and lignin (80–10). The results of lignin recovery can be seen in Table 1. In this table, it can be seen that the highest percentage of lignin recovery occurs in the lignin isolation process with a concentration of 3 M NaOH—40 mesh size of 63.36%, 8 M NaOH—60 mesh size of 75.73%, and 10 M NaOH—80 mesh size 63.79%.
No. | Concentration of NaOH (M) | Lignin (%) | |||
---|---|---|---|---|---|
mesh 40 | mesh 60 | mesh 80 | mesh 100 | ||
1 | 2 | 22.46 | 20.66 | 48.60 | 18.00 |
2 | 3 | 63.36 | 34.36 | 61.80 | 22.22 |
3 | 6 | 32.26 | 13.07 | 24.43 | 35.80 |
4 | 8 | 66.80 | 75.73 | 38.36 | 24.30 |
5 | 10 | 62.85 | 51.80 | 63.79 | 26.10 |
Results of lignin isolation at variations in bagasse size and NaOH concentrations.
Based on the results of the percentage lignin obtained and the results of the lignin functional group absorption test, it turns out that not all research variations have three indicators of the lignin-forming functional groups. The lignin results were compared by looking at the percentage transmittance value; the best lignin results were lignin (80–3), which is bagasse lignin processed with 80 mesh size variations using NaOH 3 M. Lignin (80–3) is then compared with lignin commercial standards which are lignin of Aldrich and Kraft. Figure 7 shows the FTIR test results on the sample result of isolated and sample of standard lignin.
FTIR test results on lignin isolation.
Figure 7 shows the combined FTIR results for the four most lignin isolation processes, which produce lignin yields of more than 60%. The four variations of lignin isolation are represented as curve a, curve b, curve c, and curve e. This FTIR graphic overlay is then combined with the standard lignin FTIR results, namely, curve “d” at this figure (Table 2).
No. | Typical functional group vibrations in lignin structure | Wave number (cm−1) | |||
---|---|---|---|---|---|
Standard | Bagasse lignin (80–3) | Aldrich lignin | Kraft lignin | ||
1. | Stretch the phenolic O-H | 3200–3550 | 3405.67 | 3436.62 | 3414 |
2 | Aliphatic and aromatic stretch groups ▬CH▬ | 2900 | 2919.70 | 2930.17 | 2926.01 |
3. | Stretch the arena▬C═C | 1500–1600 | 1511.92 | 1599.14 | 1614.42 |
4. | Amine C▬N | 1000–1250 | 1100 | ||
5. | Alkyl C▬H | 600–700 | 650 |
Comparison of the typical absorption peak wave numbers of bagasse lignin with commercial standard lignin FTIR spectrum by Aldrich and Kraft [35].
Based on the reference, standard lignin consists of five main components, namely, phenolic O▬H functional groups at wave number 3200–3550 cm−1, aliphatic and aromatic ▬CH▬ stretching groups at wave number 2900 cm−1, the C═C aromatic functional groups at wave number 1500–1600 cm−1, amine C▬N, and alkyl C▬H [37]. There are three main components that are the same as Aldrich lignin and Kraft lignin, namely, phenolic, aliphatic aromatic, and arenas.
In Figure 7, for the four curves that have a shape similar to the standard curve, curve “e” (colored black) shows peaks at phenolic, aliphatic, and aromatic wavelengths. So that based on the overlay of the FTIR results, it can be said that the most similar to the standard conditions is the “e” (black) curve which is the result of 80 mesh lignin isolation with 3-M NaOH reagent.
The selected lignin was then continued for the sulfonation process with several variations in the concentration of sodium bisulfite. The sulfonation process has been done with various variations in the concentration of sodium bisulfite and sulfonation time. The best results were achieved in the sulfonation process with a concentration of 0.25 M sodium bisulfite and a sulfonation time of 5 hours. Sulfonation process repeated three times and compare to find spectrum that compose lignosulfonate. The final result of the sulfonation process is lignosulfonate in the form of a light brown powder, as shown in the figure below Figure 8 (Table 3).
Sodium lignosulfonate surfactant from bagasse.
No. | Functional groups in the structure of lignosulfonates | Wave numbers (cm−1) | ||
---|---|---|---|---|
SLS standard (Patricia) | SLS standard (Aldrich) | SLS bagasse | ||
1. | Stretch alkene ═C═C | 1630–1680 | 1608.34 | 1635.34 |
2 | Stretch Sulfonate S═O | 1350 | 1365 | 1384.64 |
3. | Carboxylate C═O | 1000–1300 | 1187.94 | 1114.64 |
4. | Ester S-OR | 500–540 | 499.83 | 462.83 |
Comparison of the FTIR spectrum of SLS surfactant-synthesized bagasse and the FTIR spectrum of SLS standard Patricia and Aldrich.
From the result of FTIR test, lignosulfonate has been formed, indicated by difference a wavelength spectrum of lignosulfonates and a wavelength spectrum of lignin. The sulfonation process was done in 3 repetitions and the results were tested again by FTIR. With 3 repetitions of the process, the results are almost the same, so you can say the process is correct. To ensure the perfect result of the sulfonation process, a comparison was made with other lignosulfonates [34]. The standard lignosulfonate used for comparison were SLS Aldrich and SLS Patricia. From the FTIR results, the spectrum of SLS surfactant synthesized bagasse and sodium lignosulfonate standard spectrum, the absorption peak and its wave number in the FTIR spectrum of SLS surfactant synthesized from bagasse showed conformity with the spectrum of FTIR standard. This shows that the sulfonation process of lignin to lignosulfonate has been successfully.
In Figure 9, it is clear that there is a difference between the FTIR results of lignin and surfactant, where on the blue curve line, as in the surfactant FTIR curve, there is a shift in the absorption peak that occurs, especially at a wavelength of 1635.34 cm−1 as a function of the alkene group, at a wavelength of 1384.64 cm−1 as a function of the sulfate group, at a wavelength of 1114.65 cm−1 as a function of the carbolic acids group, and at a wavelength of 462.832 cm−1 as the ester functional group.
Overlay of FTIR surfactant—Lignin from bagasse.
Some of the peaks read on FTIR showed lignin and lignosulfonate bagasse components. The lignin component consists of phenolic functional group elements OH, aliphatic and aromatic groups ▬CH▬, C═O ketone groups, arena functional groups ▬C═C▬, CN amine groups, and CH alkyl groups with similarity values for standard spectrum wavelengths, such as those shown in Table 4 (Figure 10).
Indicator | Component | Wavelength (cm−1) |
---|---|---|
Lignin | Phenolic O-H | 3400 |
Aliphatic and aromatic ▬CH▬ | 2910 | |
Ketone C═O | 1450 | |
Arena ▬C═C | — | |
Amine C▬N | 1100 | |
Alkyl C▬H | 650 | |
Lignosulfonates | Alkene C═C | 1635.34 |
Sulfate S═O | 1384.64 | |
Carboxylic acids C═O | 1114.65 | |
Ester S-OR | 462.832 |
FTIR of lignin and lignosulfonate bagasse.
Sugarcane becomes lignosulfonate [
Likewise for lignosulfonates, with indicator components consisting of C═C alkenes, sulfate S═O, C═O carboxylic acids, and S-OR esters, with spectrum wavelengths close to the standard spectrum wavelength values. Lignin from bagasse can be completely synthesized into sodium lignosulfonate surfactant completely with lignosulfonate components consisting of alkene, sulfonate, carboxylate, and ester.
Furthermore, from the results of the NMR test, the components form the lignosulfonate. In the HMQC data, it can be seen that the proton nuclei are directly correlated with carbon-13 (13C) or have one bond (1JC, H) so that their own pairs can be known with certainty. The broad singlet signal on the δ H 6.64 ppm chemical shift (2H, bs, H−3, and H-5) correlates directly with carbon at δ C 102.2 ppm (C-3 and C-5). In addition, the HMQC spectrum also indicates the presence of methylene protons bound to C-9, methane bound to oxygen, and sulfate bound to C-8 and C-7, respectively.
From the HMBC spectrum, it can be seen that there is a correlation between protons and carbon with a distance of two bonds (2 J) to three bonds (3 J), which can be seen in Figure 3. From the HMBC data, it can be seen that there is a correlation between H-3 and H-5 with C-5/C-3, C-1, and C-7; H-7 correlates with C-8 and H-9 correlates with C-8 and C-7. These data support the existence of phenyl propanoid compounds as the basis for lignosulfonates [38]. The correlation between HMQC and HMBC can be seen in Figure 11. With the results that look like this, it shows that the isolation process of lignin from bagasse has been successful. Likewise, the sulfonation of lignin to lignosulfonate has also been successful.
NMR test results—HSQC and HMBC correlation of bagasse lignosulfonate H4S4 isolates.
Based on the results of the lignin sulfonation process on lignin sulfonation optimization, several conclusions can be drawn, namely:
Bagasse as biomass is a raw material that can be processed into lignosulfonate surfactants. The lignosulfonate obtained from bagasse is processed in two stages, namely, the lignin isolation process using sodium hydroxide and the sulfonation process using sodium bisulfite.
Based on the FTIR test, the lignin-forming components were shown by the presence of phenolic functional groups O▬H, aliphatic ▬CH▬ and aromatic stretching groups, and C═O ketone functional groups, while the lignosulfonate-forming components were indicated by the presence of alkene groups, sulfate groups, and carbocyclic acids and ester functional groups, each with a spectrum wavelength corresponding to the standard spectrum.
Based on the results of the NMR test, the presence of phenyl propanoid compounds as the basis of the lignosulfonate compounds indicates that the sulfonation process has reached the expected target, namely, the formation of lignosulfonates completely.
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Dr. Koprowski has authored more than a hundred research papers with dozens in impact factor (IF) journals and has authored or co-authored six books. Additionally, he is the author of several national and international patents in the field of biomedical devices and imaging. 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His fields of interest are anterior segment disease, keratoconus, glaucoma, corneal dystrophies, and cataracts. His research topics include\nintraocular lens power calculation, eye modification induced by refractive surgery, glaucoma progression, and validation of new diagnostic devices in ophthalmology. \nHe has published more than 100 papers in international and Italian scientific journals, more than 60 in journals with impact factors, and chapters in international and Italian books. 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