Alzheimer’s disease versus dementia and normal aging [6, 7].
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Hincapie and Javier E. Sierra",coverURL:"https://cdn.intechopen.com/books/images_new/913.jpg",editedByType:"Edited by",editors:[{id:"72042",title:"Dr.",name:"Roberto",surname:"Hincapie",slug:"roberto-hincapie",fullName:"Roberto Hincapie"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},onlineFirst:{chapter:{type:"chapter",id:"80735",title:"Alzheimer’s Disease: An Insightful Review on the Future Trends of the Effective Therapeutics",doi:"10.5772/intechopen.102762",slug:"alzheimer-s-disease-an-insightful-review-on-the-future-trends-of-the-effective-therapeutics",body:'Alzheimer’s disease (AD) is a brain disorder described in 1906 by Aloes Alzheimer, a German physician [1]. It is a progressive and neurodegenerative disorder which mainly occur in old aged people of over 65 years of age [1, 2, 3]. For progression and development of disease various pathways are involved such as formation of plaque, inflammatory cascade, cholinergic deficit, oxidative stress, and many more. Senile plaques formation and neurofibrillary tangles persist significant neuro-pathological symbols of this disease. Senile plaques are the main component of amyloid beta (Aβ) peptide that are covered by dystrophic neurites and activated microglia. Accumulation of Aβ results changed process of proteolytic amyloid precursor protein (APP) through beta and gamma secretase. The β-amyloid peptide, with 39–42 amino acid residues (BAP), perform vital role in development of AD. There are mainly two types of AD, familial AD which affects the people who have age less than 65. The other type of AD is sporadic AD which affect the people older than 65. At present there is no cure for Alzheimer’s disease but it could me managed to some level by using available medications (Table 1) [4, 5].
Factors | Dementia | Alzheimer’s disease | Normal aging |
---|---|---|---|
Definition | CNS disorder due to disease or any other pathological condition. | Common form of dementia. | Condition occur due to programmed cell death with time (gene therapy) and causes various disability. |
Cause | AD, stroke, thyroid issues, vitamin deficiency, etc. | Deposition of beta amyloid protein in brain. | May cause biological systems to fail (DNA oxidation, DNA methylation, and apoptosis). |
Duration and age | Permanent damage and 65 years and olders. | Average 8–20 years and 65 year but can occur as early as 30s. | Gradual and progressive condition until death. |
Symptoms | Issues with memory, poor judgment, less focus and attention. | Difficulty to remembering newly learned information. | Bone break more easily, decrease overall energy, greater risk of heart stroke or hypothermia. |
In 2020 approx. 50 million individual dealing with dementia worldwide. In India more than four million of people suffering from AD and dementia while in USA approx. 5.8 million living with dementia and AD. It is estimated that it is the fifth main source of death in USA and the number of death increased 146% between 2000 and 2018. It is predicted the causality will increase to 13.8 million which number of patient increases to 13.5 million by 2050. Elderly persons are more prone to younger one [8].
In maximum case genetic lifestyle choices aging stress and environmental factors induces AD [9].
Researchers have claimed that older adults have more risk of having AD. Scientists are still learning, how age-related changes in the brain may harm neurons and contribute to Alzheimer’s [10].
It occur due to mutation in chromosome 1, 14, and 21. The changes on chromosome 1 produces PRESENILIN-2 (PSEN2) named protein while chromosome 14 produces PRESENILIN-1 (PSEN1). These PSEN 1 and PSEN 2 directly and indirectly both trigger/encode for membrane protein convoluted for amyloid precursor protein. These mutations reduce the effectiveness of γ-secretase, an enzyme which is responsible for formation of beta amyloid peptide (βAP) [11]. Amyloid precursor protein is coded on chromosome 21 and this mutation results in overproduction of beta amyloid peptide. Mutation on chromosome 1, 14, and 21 results in early onset AD [12].
Apo-lipoprotein E (APOE) gene is responsible for late onset AD. APOE gene is lipid metabolism regulator which have an affinity for beta amyloid protein and increases the risk of AD. Chromosome 19 produces APOE gene. The inheritance of APOEe4 allele own genetic risk in sporadic AD. APOEe4 allele, age elevate the risk for development of late AD by two to three folds and two copies of five folds [13].
Variations in gene for receptor sortilin, SORT1, that is important for transferring APP from surface of cell to Golgi-endoplasmic reticulum complex, have been found in familial and sporadic types of AD [14].
Conditions such as heart disease, stroke, high blood pressure, diabetes, and obesity are also linked as risk factors for AD [15].
The real origin of this disease is not well known but problems are linked with brain protein that work abnormally and cause malfunction. As a result neurons were damaged then fail to connect other neuron as a result they die. Initially the degradation starts within the region of brain which control memory ultimately dementia occur (Figure 1) [16].
Clinical findings in Alzheimer’s disease [
In the initial stage of AD amyloid proteins works abnormally and cause overproduction of beta amyloid secretase named enzyme split amyloid processor protein and due to deviation from this process, especially sudden change in gamma and beta secretases leads to unnatural production of amyloid beta [18].
Tau protein is known for its stabilizing property. It is useful in the transportation of nutrients and others essential matter within the neurons while in AD. Tau protein cause mutation and changes its structure which is known as neurofibrillary tangles [18, 19].
It is observed in the patient of AD there is deficiency of ACh due to abnormal functioning of choline acetyl transferase. This will treat as a clinical hallmark to support cholinergic hypothesis there is also a possible treatment of AD by increasing the level of ACh by reducing the activity of AChE cholinergic depletion observed after neurodegenerative cascade various cholinesterase inhibitors currently used in the treatment of AD [20].
It is defined as the excess interaction of neurotransmitter glutamate and other excitatory neurotransmitter which may act as a potent neurotoxins for Alzheimer [21].
Apo-lipoprotein E play important role in the cholesterol transportation and catabolism of triglyceride lipoprotein. Cholesterol also alter the clearance of amyloid beta and generation of NFT in neuronal membrane APOE4 also enhance the deposition of beta amyloid protein. High level of cholesterol in brain there by alter the member functioning this leads to plaque formation resulting AD [22].
Oxidative stress is generated due to imbalance of ROS generation and its quenching. Brain is more prone for oxidative stress due to high consumption of O2. High level of polyunsaturated fatty acid. Low level of antioxidants and high level of redox transition metal ions. These all factors facilitate the production of reactive oxygen species like superoxide, hydrogen peroxide, etc. These ROS interact with surroundings proteins nucleic acids, etc. and cause cellular dysfunction [23]. There is also a close relationship between amyloid beta and oxidative stress because amyloid beta elevate the formation of ROS and initiate mitochondrial damage. This will also cause oxidative damage. These effects can also be observed in brain of triple transgenic mouse model of AD where tocopherol and GSH level decrease while lipid peroxidation is increased [24]. However this was observed before any plaque formation. While in another model dual mutant APP was expressed, oxidative stress and inflammation was induced by thiamine deficiency provoke plaque formation and enhance the level of amyloid [25].
It is observed in the marphotric analysis of AD patients brain showed significant deficiency of mitochondria while its DNA and protein concentration elevate in cytoplasm and in the vacuoles associated with lipofuscin [26]. These mitochondria may be damaged due to autophagy and oxidative stress. Mitochondrial cytochrome oxidase activity also reduced in cortical region of AD brain. Due to this deficiency mitochondrial dysfunction occur and ROS generated and energy stores were decreased and ultimately neurodegeneration occur [27].
Evidence from animal and human studies support functional roles of sex hormones like estrogens, progesterone, and androgens in behavior and cognition. With several neuroprotective activity involved, age reduces level of sex hormones were connected with greater possibilities of cognitive degeneration and AD. For example, in females development of AD is associated with decreased exposure to estrogens across the lifetime, while in males age related degeneration in both levels of peripheral and brain testosterone is linked with greater susceptibilities of AD development. Also, alterations in receptors of sex hormone and downstream signaling pathways during aging have been stated. For example, the nonfunctional splicing estrogen variants receptor alpha in the hippocampus was enhanced throughout aging and AD, with advanced levels in female old age subjects in comparison to males. Moreover, studies recognized polymorphisms of estrogen receptors related with intellectual decay and AD development in females, especially in APOE ε4 (APOE4) transporters. These information recommended diminished responsiveness of brain to sex hormones during aging and disease development. However, clinical trial outcomes of sex hormone therapy in AD are rather contentious. Despite prior studies associating protective activity of estrogen replacement against AD in females, huge clinical studies failed to exhibit any useful possessions. It was suggested that replacement of hormone initiation in the serious window of perimenopause may diminish the risks of dementia, while it might raise the risks if started a very long time after menopause. Moreover treatment timing, reduced responsiveness at receptors of brain and downstream signaling pathways might add to the uselessness of hormonal therapy. Together, these investigations recommend the complication of sex hormones association in AD [31].
Currently there is no cure for this disease, the objective of several medicine is used to reduce symptoms linked with disease and to reduce disease progression (Table 2) [32, 33, 34, 35, 36].
Drug name | Indication | Mode of action | Adverse effect |
---|---|---|---|
Donepezil | Minor to chronic | It stops the breakdown of ACh by preventing the function of acetyl cholinesterase | Fatigue, abnormal dreams, hallucinations, confusion, hypertension, abdominal pain |
Treats intellectual indication of AD | |||
Galantamine | Minor to medium | Stops the breakdown of Ach and stimulates receptors to discharge extra ACh | Somnolence, bradycardia, insomnia, urinary tract infection, anorexia, syncope |
Treats intellectual indication of AD | |||
Rivastigmine | Minor to medium | Stops the breakdown of Ach by preventing the enzymes that abolish ACh | Dizziness, diarrhea, anxiety, vertigo, asthenia, tachycardia |
Also used to treat dementia from Parkinson’s disease | Treats intellectual indication of AD | ||
Memantine | Medium to severe | Blocks glutamatergic (NMDA) receptors and controls the action of glutamate | Headache, constipation, vomiting, backache |
Treats intellectual indication of AD | |||
Donepezil/memantine | Medium to severe | it binds to NMDA receptor-operated caption channels, and gives therapeutic effects by preventing persistent stimulation in CNS | Hallucination, headache, cough, fatigue, cramping, syncope, increased frequency of bowel movements |
Currently used drug for the treatment of Alzheimer’s disease.
From the previous eras, the pharmaceutical industry has decided to chiefly focused on the amyloidocentric method, dedicating significant possessions to form useful AD drugs. Nevertheless, numerous failures of drug candidates in clinical trials have led investigators to question the viability of this approach [10, 11, 12]. Possible cause for failure is a absence of biomarkers that could consistently recognize AD in comparatively initial phases. It is totally promising that the patients presently enrolled for phase III trials are in such advanced phases of AD that any attempted interference is possibly inadequate. In the meantime, there is still a number of new management under development, that focused the amyloidogenic route. In order to decrease generation of Aβ from the APP, inhibition of γ- and β-secretase and the potentiation of activity of α-secretase have been deliberated.
β-secretase enzyme complex contributes in the primary phases of the amyloidogenic APP-processing pathway. The inhibitors of β-secretase development is a task because, besides the APP, this complex has several substrates. To give just one example, neuregulin-1, that included in the CNS axons myelination and synaptic elasticity, is a target β-secretase. Substrates wide range results to substantial adverse effects, even if the precise enzyme inhibition is reached. But, E2609 (clinical trial ID# NCT01600859), MK-8931 (NCT01739348), and LY2886721 (NCT01807026 and NCT01561430) have all exposed efficiency in decreasing the production of Aβ by up to 80–90% in the cerebrospinal fluid (CSF) in humans. None of inhibitors of β-secretase have touched the market so far [37, 38, 39, 40].
In the final stage of amyloidogenesis, γ-secretase complex is responsible for the production of Aβ(1–40) and Aβ(1–42). Inhibition of γ-secretase was firstly proposed strategy for the management of Alzheimer’s disease but the substrate promiscuity shows equal issues facing γ-secretase inhibitors. γ-secretase proposed to target the Notch protein which is responsible for the regulation of cell proliferation, development, differentiation and cellular communication but off target secondary effects are major concern [41, 42, 43].
Semagacestat (LY450139) named γ-secretase inhibitor reduces the Aβ level in the blood and in cerebrospinal fluid [44]. The results obtained from the clinical study conducted on 3000 patients shows the major adverse effects like decrease cognition abilities and difficulty in the carry out daily living activities and elevated skin cancer incidence and increased risk of infection and weight loss. Another γ-secretase named avagacestat discontinued in the development stage due to lack of efficacy (NCT00810147, NCT00890890, NCT00810147, NCT01079819, [45, 46, 47]).
Several nonsteroidal anti-inflammatory drugs like indomethacin, ibuprofen, flurbiprofen, sulindac also decreases the Aβ(1–42) peptide levels in in-vivo and in in-vitro studies. Ibuprofen is a cyclooxigenase inhibitor while R-flurbiprofen (tarenflurbil) is not, so the reduction of Aβ(1–42) peptide levels is not associated with the COX inhibition. Unfortunately, in clinical trials tarenflurbil and ibuprofen does not shows efficacy for the treatment of Alzheimer’s disease. The idea of long term use of NSAID’s for the treatments of Alzheimer’s disease as NSAIDS reduces the Aβ peptide level in blood but negative results reported in the clinical studies that’s why this hypothesis requires further investigations [48, 49].
Clinical studies with 8-hydroxiquinolines compounds like clioquinol and PBT2 also conducted for the treatment of Alzheimer’s disease. The mechanism of action is yet established, but the expected MOA suggested that the increased levels of oxidative stress is due to the copper ions binding to Aβ, leading to metal-mediated generation of ROS (reactive oxygen species). It is proposed that the 8-hydroxiquinolines may prevent Aβ aggregation and restoring homeostasis in the cellular levels of copper and zinc ions. But after in clinical development these compounds failed due to lack of efficacy [50, 51, 52].
Another possible treatment choice that is involved on the amyloidogenic pathway is to stimulate the existing amyloid aggregates clearance. To achieve this, three different approaches have been assessed.
Amyloid plaques are destroyed by various proteases comprising neprilysin, IDE, plasmin, angiotensin converting enzyme, endothelin converting enzyme, and metalloproteinases. Levels of protein these enzymes reduces in AD, that promotes accumulation and formation of Aβ. Despite being an attractive approach for forming disease-modifying medicine, no compounds with this MOA have ever entered advanced clinical development because of lack of specificity.
Transport of Aβ between the circulation of CNS and peripheral is controlled by: (i) apolipoproteins (e.g., Aβ might be transported from the blood to the brain when it is bound to APOE); (ii) low-density lipoprotein receptor-related protein (LRP-1), that enhances Aβ discharge from the brain to the blood; (iii) receptor for progressive glycation end products (RAGE), that enables the Aβ transport across the blood-brain barrier (BBB) [53, 54].
Any treatment goal, that is determined on this mechanism, is to decrease the load of cerebral amyloid by trying to control Aβ to the peripheral circulation. To this end, a different number of approaches have been suggested, particularly the administration of LRP-1 peripherally. Though, the only drug candidates that have entered the clinical phase are the RAGE inhibitors.
Immunotherapy approach designed to stimulate clearance of Aβ with the aimed of decreasing load of amyloid load in AD. Active immunization (vaccination) with either Aβ(1–42) (main form found in senile plaques) or other synthetic fragments has been positively assessed in transgenic mouse models of AD. Human tests were primarily hopeful; though first-generation vaccine (AN1792) treatment has shown major adverse events which results to the phase II trials cessation. AN1792 contained of a synthetic full-length Aβ(1–42) peptide with a QS-21 adjuvant. Because of a T cell-mediated autoimmune response, 6% of patients have established inflammation in brain that ended up being aseptic meningoencephalitis [55].
Second-generation vaccines were planned utilizing a limited portion of Aβ(1–6) peptide in an try to inhibit nonspecific immune response seen with the full-length vaccine. Novartis designed CAD 106, was the first second-generation vaccine which moved to development phase. Newly finished phase II trial have exposed a Aβ-specific antibody response in 75% of treated patients, without producing any side effect. Janssen developed ACC-001, has freshly finished two-phase II trials (NCT01284387 and NCT00479557) with an additional phase II trial still continuing (NCT01227564). Though, the pharmaceutical industry has canceled the ideas for this vaccine development. Further vaccines, comprising tetra-palmitoylated Aβ(1–15) re-formed in a liposome (ACI-24), MER5101 and AF205 are now in different phases of preclinical progression [56, 57, 58].
It is the monoclonal or polyclonal antibodies administration directed against Aβ. This treatment contains intravenous administration of anti-Aβ antibodies to the patient. The advantage of this approach is to match to active immunization is which the proinflammatory T cell-mediated immune response should not arise. Reports have shown that in transgenic animals passive immunization decreases the load of cerebral amyloid and recovers cognition, even when the amyloid plaque numbers are not suggestively decreased. This could be recognized to the soluble amyloid oligomers neutralization, that progressively identified to play an important role in the pathophysiology of AD.
Bapineuzumab and solanezumab are two monoclonal antibodies which are reach now present in advanced phase of development. Though, two phase III trials had failed in 2012 due to low effectiveness in patients with mild-to-moderate AD [59]. Both are humanized monoclonal antibodies against Aβ(1–6) and Aβ(12–28), respectively. In bapineuzumab, noteworthy decrease in brain amyloid plaques and phosphorylated Tau in cerebrospinal fluid was stated. Though, the treatment unsuccessful to give noteworthy developments of brain function. In a solanezumab trial, infusions of 400 mg of solanezumab or placebo were given for 80 weeks once a month in patients with mild-to-moderate AD. The outcomes recommended that solanezumab might recover cognition in mild AD; but statistical significance was not attained in study. Presently solanezumab present in phase III trials in patients with AD (NCT01127633 and NCT01900665) and in older persons who have common thinking and memory function but who might be at danger of AD developing in the future (NCT02008357, [60, 61]).
Crenezumab (MABT5102A) is a humanized monoclonal antibody that uses IgG4 backbone. In April 2014 a stage II trial to measure the safety and effectiveness in patients with mild-to-moderate AD (NCT01343966) was accomplished, while the outcomes are not yet openly accessible. The supreme stage II trial pointing to assess the safety and effectiveness of crenezumab in asymptomatic transporters of E280A autosomal-dominant mutation of PSEN1 initiated in November 2013 (NCT01998841).
Other monoclonal antibodies against Aβ established so far contain PF-04360365 (ponezumab) that targets the free carboxy terminal amino acids 33–40 of the Aβ peptide; MABT5102A, that binds to Aβ monomers, oligomers, and fibrils with similarly great affinity; GSK933776A, that is likewise to bapineuzumab in which it binds to the N-terminal Aβ(1–5). Additional, other passive immunotherapies typically in stage I clinical trial involve NI-101, SAR-228810, and BAN-2401 [58, 62].
In neurons Tau proteins are extremely soluble and abundant where they play a important role in stabilization of microtubule, mainly in axons [63]. Tau hyperphosphorylation resulting the insoluble paired helical filaments (PHF) development that form neurofibrillary tangles. The microtubule-binding capacity damage initiate destabilization of cytoskeleton, that ultimately develops neurodegeneration and neuronal death [64]. As a substitute to amyloidocentric strategies, this treatments goal to prevent the phosphorylation of Tau protein. Additional, microtubule-stabilizing drugs can be utilized as a disease-modifying approach in AD. In current years, immunomodulation was recommended as a feasible choice for stimulating operative Tau aggregates clearance [65].
All Tau proteins are a result of different splicing of a microtubule-associated protein Tau (MAPT) gene. Primary mechanism that controls Tau binding to microtubules is phosphorylation. The protein remains soluble under physiological circumstances; though, in this disease, pathological hyperphosphorylation of Tau compromises its regular functions [66, 67]. Imbalance between the catalytic activity of kinases and phosphatases occurs hyperphosphorylation. Enhanced expression of active forms of several kinases in the areas proximal to neurofibrillary tangles has been labeled in AD, comprising CDK5, GSK3β, Fyn, stress-activated protein kinases JNK and p38, and mitogen-activated protein kinases ERK1 and ERK2 [68]. Certain kinases promote continuation of tau phosphorylation in neurofibrillary tangles. Resulting, noteworthy research determinations have been dedicated to the kinase inhibitors development as a probable treatment approach for AD. For example, SP600125, a extensively utilized pan-JNK inhibitor, employs valuable effects on cognition and decreases neurodegeneration in an APP/PS1 transgenic mouse model of AD. It has been planned which precise inhibition of JNK3 can be adequate to carry comparable benefits as seen with SP600125 in rodent models. Human data in AD patients designate a positive correlation between the JNK3 and Aβ(1–42) levels in the brain. Moreover, JNK3 upregulation was distinguished in the CSF and was related with loss of memory. Consequently, inhibition of JNK3 remains a capable goal for future treatments [69, 70, 71].
Tau hyperphosphorylation contribute to neurotoxicity detected in AD brain. Methylene blue dye derivatives have revealed certain potential Tau aggregates formation inhibition. Methylene blue disturbs the Tau aggregation, has the capability to prevent amyloid aggregation, recovers the effectiveness of mitochondrial electron transport chain, decreases oxidative stress, stops mitochondrial impairment, and is also an autophagy modulator. The first-generation molecule resulting from methylene blue (Rember) seemed to stabilize AD development in a clinical trial that continued 50 weeks. These outcomes encouraged investigators to form a next-generation form of methylene blue, TRx 0237. This agents is a purified derivative of methylene blue that not only prevents aggregation of Tau protein but also liquefies brain tau aggregates. Various trials are presently ongoing (NCT01626391, NCT01689233, NCT01689246, NCT01626378) to assess the possible effectiveness of this agent in AD [72, 73].
Stabilization of microtubule might possibly attain a comparable end-result as which seen with the Tau hyperphosphorylation inhibitors. Paclitaxel is a microtubule-stabilizing agents presently in utilize in the oncology arena. Inappropriately, this agents is unable of BBB crossing and its utilize is related with major adverse events, that limits its efficacy in AD. In addition to paclitaxel, other microtubule-stabilizing agents like TPI 287 have been measured as a probable AD remedy. TPI 287 is a derivative of taxane, also utilize in the treatment of cancer. TPI 287 alleviates the microtubules by binding to tubulin. NCT01966666 trial will estimate TPI-287 safety, pharmacokinetic possessions, and tolerability by intravenous infusion in mild-to-moderate AD.
Epothilone D is a microtubule-stabilizing agent that enhanced axonal transport, decrease axonal dystrophy, reduced Tau neuropathology, and decreased hippocampal loss of neuron; though, in 2013 drug development for AD was discontinued after an unsuccessful clinical trial. With respect to Tau, more research are essential in order to better understand the exact molecular mechanisms elaborate in neurotoxicity of Tau. Current research associating the neurotoxic profiles of different forms of Tau recommend which is a soluble form is probable the greatest toxic. Thus, future therapeutic approaches should be focused on aiming Tau soluble forms [74].
Just as with the immunotherapies aiming Aβ, both passive and active immunization approaches against Tau have been measured. It was established that decrease in formation of Tau aggregate and enhanced Tau oligomers clearance and insoluble aggregates could all be reached with either active or passive immunotherapies. In rodents, treatment with monoclonal antibodies directed against hyperphosphorylated Tau has results to improvements in cognition and was not connected with noteworthy side effects.
Axon neuroscience began a stage I trial in 2013 to estimate the safety and tolerability of AADvac-1, an active immunotherapy that contains synthetic peptide derived from the Tau sequence coupled to keyhole limpet hemocyanin; the precise molecular nature of the antigen has not been disclosed (NCT01850238 and NCT02031198). AADvac-1 uses aluminum hydroxide as an adjuvant. At the 2014 Alzheimer’s Association International Conference (AAIC) in Copenhagen, good preclinical safety profile was reported for the treatment period of up to 6 months in rats, rabbits, and dogs. These initial outcomes are hopeful and it remains to be seen whether AADvac-1 will prove satisfactory safety and efficiency in patients [75, 76].
The hippocampus, the chief region of brain elaborate in memory processing, is influenced by modulation of cholinergic neurotransmitter. One of the well categorized irregularities linked with neurotransmitter deviations is the cholinergic neurons degeneration in the nucleus basalis of Meynert and the cholinergic inputs loss to the neocortex and hippocampus. Various studies reported reduced in choline acetyltransferase (ChAT), acetylcholine (ACh) release, as well as decreases in nicotinic and muscarinic receptors in the cerebral cortex and hippocampus of postmortem AD brains. Acetylcholinesterase inhibitors (AChEI), one of the only two classes of compounds that presently accepted for AD treatment, act by stimulating ACh bioavailability at the synapse. Inappropriately, none of these agents are proficient of withdrawing the course of AD nor of even noticeably reducing down the degree of disease development. Their clinical effect is basically palliative; though, their possible utilize in combination therapy with other disease-modifying agents should not be omitted [77, 78].
As revealed by clinical study data and research articles that diabetes is a one of the key factor that leads to AD pathology and unfolds the close connection between insulin-deficient diabetes and cerebral amyloidosis. These data also suggests about insulin signaling impairments (both peripheral and central) is possibly be existing in both diseases. Hence, considering insulin hormone at the core, “type 3 diabetes” hypothesis of AD was developed, observing metabolic phenotypes into a coherent framework [79].
The most anticipated mechanisms for the development of AD due to diabetes could be: glucose toxicity, insulin resistance, oxidative stress, elevated levels of advanced glycation end products, and cytokine-mediated neuroinflammation. Recently, Clarke and colleagues demonstrated that neuroinflammatory cascades can be initiated by the administration of soluble hypothalamic Aβ oligomers that ultimately causes disturbances in peripheral glucose homeostasis. Tumor necrosis factor α (TNFα) may have a significant role during this process [80].
Rosiglitazone and pioglitazone are used as antidiabetic drugs, which regulate glucose homeostasis by increasing insulin sensitivity, reducing blood glucose levels, and improving lipid metabolism. Both compounds have also been studied as potential therapeutics for AD treatment, with reported improvements in mitochondrial oxidative metabolism [81]. In animal models, pioglitazone modified various indices of brain aging but did not slow down the cognitive decline. Rosiglitazone and pioglitazone also induce the expression of peroxisome proliferator-activated receptor-γ co-activator 1 alpha (PGC-1α), a molecule that plays multiple roles in mitochondrial biogenesis, energy metabolism, and mitochondrial antioxidants expression. Previous studies have demonstrated that, in the human brain tissues, the expression of PGC-1α decreases with progression of AD dementia. Thus, PGC-1α upregulation may improve the mitochondrial energy metabolism and AD pathology [82, 83, 84, 85, 86].
In a small scale clinical trial on mild-to-moderate AD patients, it was found that pioglitazone enhances memory and cognition. On the other hand clinical trial (phase II) with larger group of patients (who did not possess an ApoE4 allele) were on treatment with rosiglitazone (6 months) shows improvement in memory retention and attention. However, similar study (phase III trial) using rosiglitazone failed to show efficacy in AD (NCT00550420). It is important to note that rosiglitazone was administered at much lower dosage than required to exert efficacious effects on AD pathophysiology in these trials, in rodent models of the disease. NCT00348140 recently completed clinical trial in which rosiglitazone was administrated in combination with AChEIs in patients with AD (mild-to-moderate) and until now no further outcome yet reported.
As a treatment possibility for AD, intranasal insulin have also been considered as it bypasses the BBB easily; adding the advantage of possibly minimum adverse events in peripheral tissues. Theoretically it is well established that direct delivery of insulin to the brain will activate cerebral insulin signaling leading to enhancements in memory processing resulting into neuroprotection. A recent ongoing clinical trial (with NCT017679090 is assessing long-term (12 months) efficacy of intranasal insulin (Humulin R U-100) among mild AD patients [87].
Also, it has been found that reduced plasma amylin concentrations may contribute in the progression of AD. As revealed by transgenic animal models of AD, amylin and pramlintide (amylin analog) reduced the brain Aβ levels and advances cognition. Interestingly, amylin inhibits β-secretase, whereas pramlintide did not [88].
Here is the number of herbal plants reported to might have anti-Alzheimer activity (Table 3).
Sr. No. | Work done | Plant used | Common name | Author | Year | Ref. |
---|---|---|---|---|---|---|
1. | Effects of the hydroethanolic extract of | Fir clubmoss | Valu et al. | 2021 | [89] | |
2. | Evaluation of traditional herb extract | Sage | Datta et al. | 2020 | [90] | |
3. | Protective effects of tenuifolin isolated from | Yuan zhi | Wang et al. | 2019 | [91] | |
4. | Shankhapushpi | Kizhakke et al. | 2019 | [92] | ||
5. | Cheeseweed | Jiménez et al. | 2019 | [93] | ||
6. | Antioxidant, anti-Alzheimer and anti-parkinson activity of | Indian wormwood | Pal and Pradeep | 2018 | [94] | |
7. | Antioxidant and anti-acetylcholinesterase activities of essential oils from garlic ( | Garlic | Akinyemi et al. | 2018 | [95] | |
8. | Nootropic activity of ethanolic extract of | Ankol | Parameshwari et al. | 2018 | [96] | |
9. | Drumstick tree | Mahaman et al. | 2018 | [97] | ||
10. | Ameliorative effect of | Shonna cabbage | Manasa et al. | 2017 | [98] | |
11. | Evaluation of nootropic activity of green peas in mice | Green peas | Kaura et al. | 2017 | [99] | |
12. | Ameliorative effect of | Celery | Phetcharat et al. | 2017 | [100] | |
13. | Evaluation of effect of alcoholic extract of | Guduchi | Jyothi et al. | 2016 | [101] | |
14 | Effect of | Green tea | Mahmoodzadeh et al. | 2016 | [102] | |
15. | Evaluation of nootropic activity of | Turmeric | Reddy et al. | 2015 | [103] | |
16. | Effect of ethanolic seed extract of | Orchid tree | Nemalapalli et al. | 2015 | [104] | |
17. | Mora | Kim et al. | 2015 | [105] | ||
18. | Anticholinesterase and antioxidant properties of aqueous extract of | Cola nut | Oboh et al. | 2014 | [106] | |
19. | Antiamnesic effect of piracetam potentiated with | Aamla | Ramachandran et al. | 2013 | [107] | |
20 | Antiamnesic activity of | Jamun | Alikatte et al. | 2012 | [108] | |
21 | Acetylcholine and memory-enhancing activity of | Cluster fig | Faiyaz et al. | 2011 | [109] | |
22 | Protective effect of | Noni | Muralidharan et al. | 2010 | [110] |
Plants studied in Alzheimer’s disease.
In 2021 USFDA approved
It was approved for medical use in the United States. Aducanumab has since been approved by the Ministry of Health and Prevention in the United Arab Emirates as of October 3, 2021, making it the second country in the world to approve the treatment.
It is suggested for mild cognitive impairment (MCI) or mild dementia stage of Alzheimer’s disease [112, 113].
Here is the figure that shows the agents which is in developing stage involve in the trials for the management of Alzheimer’s disease. Most of agents in the trial target disease modification [114] (Figure 2).
Drugs in clinical trials for treatment of Alzheimer’s disease in 2021. In which the shape of icons shows the population involve in trials; the outer ring shows drugs in Phase I; the middle rings shows drugs in Phase II; the inner most ring shows drugs in Phase III trials [
In which the shape of icons shows the population involve in trials; the outer ring shows drugs in phase I; the middle rings shows drugs in phase II; the inner most ring shows drugs in phase III trials [115].
Alzheimer’s disease is serious brain disorder, at present there is no cure for this disease but currently it can be controlled by using a drugs which symptomatically treat AD. AChE inhibitors are the first approved anti-AD drugs by the FDA, and they are also the first and the most useful drug used in the clinical treatment of AD. But now few of drugs also approved by USFDA in 2021 for the treatment of AD and few also in the trial phase. Results from clinical studies have shown different new drugs in pipeline and various novel approaches may also beneficial for treating AD. Interests in the utilization of different herbal products also increase day by day. This study provides the details about recent advancement the medicinal plants against the Alzheimer’s disease. Availability of these new medicinal plants for AD will further increase the treatment options and thus provide a significant benefit to patients who remain uncontrollable to existing therapy.
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
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The results of the research suggest fewer incorrect responses in children with ASD and in different areas compared with children with typical development. 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Telling personal stories, such as talking about your day or recounting what happened in the playground, is essential for communication and establishing relationships. However, due to their language impairments, people with aphasia (PWA) and children with developmental language disorder (DLD) often have problems with everyday discourse which impact on their lives more widely. While improvement in language skills is supported by speech-language pathology (therapy), it tends to focus on smaller linguistic components, such as single words and sentences. This chapter outlines how speakers construct discourse in everyday situations and focuses on the meanings that people use discourse to convey, as well as the lexical and grammatical resources they use to convey these meanings. Current methods for discourse analysis will be outlined and key developments in narrative discourse production therapy will be reviewed.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Lucy T. Dipper and Madeleine Pritchard",authors:[{id:"201158",title:"Dr.",name:"Lucy",middleName:null,surname:"Dipper",slug:"lucy-dipper",fullName:"Lucy Dipper"},{id:"208542",title:"Dr.",name:"Madeleine",middleName:null,surname:"Pritchard",slug:"madeleine-pritchard",fullName:"Madeleine Pritchard"}]},{id:"56698",doi:"10.5772/intechopen.70107",title:"Risk Factors for Speech-Language Pathologies in Children",slug:"risk-factors-for-speech-language-pathologies-in-children",totalDownloads:1604,totalCrossrefCites:2,totalDimensionsCites:5,abstract:"Risk factors are understood to encompass “aspects of individual behavior or lifestyle, environmental exposure, hereditary or congenital characteristics that are associated with a health related condition”. These are conditions that increase the chances of the child presenting speech-language disorders and that can be avoided, controlled, or treated. Risk is defined as the chance of a child exposed to certain factors (environmental or biological) to acquire or develop speech-language disorders. The objectives of the present study were: to identify the risk factors for speech-language disorders in children up to five years of age and to verify the relationship between risk factors and speech-language diagnostic hypotheses. The aspects of being male gender, prematurity, shyness, being an only child or youngest child, presenting deleterious oral habits, having a family history of speech-language disorders, and use of licit or illicit drugs during pregnancy seem to be the factors that should draw the attention of the health professionals in child development. Therefore, the monitoring of children who have these risk factors should be performed in order to promote the necessary stimulation and the construction of healthy environments.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Daniela Regina Molini-Avejonas, Laís Vignati Ferreira and Cibelle\nAlbuquerque de La Higuera Amato",authors:[{id:"38599",title:"Prof.",name:"Daniela",middleName:null,surname:"Molini-Avejonas",slug:"daniela-molini-avejonas",fullName:"Daniela Molini-Avejonas"},{id:"204612",title:"Prof.",name:"Cibelle",middleName:null,surname:"Amato",slug:"cibelle-amato",fullName:"Cibelle Amato"},{id:"210543",title:"Ms.",name:"Laís",middleName:null,surname:"Ferreira",slug:"lais-ferreira",fullName:"Laís Ferreira"}]},{id:"56281",doi:"10.5772/intechopen.70106",title:"Remote Speech-Language Intervention, with the Participation of Parents of Children with Autism",slug:"remote-speech-language-intervention-with-the-participation-of-parents-of-children-with-autism",totalDownloads:1530,totalCrossrefCites:1,totalDimensionsCites:4,abstract:"The question about the possibility of identifying the best therapeutic approach for children with autism spectrum disorder (ASD) has also been discussed in the literature. The intervention should be individualized, in order to involve the current level of development of the child and to identify the profile of the facilities and difficulties of each child. The families are constantly involved in complex and changeable context and are aware of the importance of access and participation to the treatment chosen, since that service delays can directly affect efficacy. In general, studies on language acquisition and development in autism focus on the child’s communication, and some analyze the mother seeking to understand how the role of parents and caregivers influences the communication of the children with autism. Observing the importance of the active inclusion of parents in the speech and language therapy of children with ASD, a Distance Speech Therapy Intervention project, was developed that would allow language stimulation of a greater number of children and adolescents with autism.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Milene Rossi Pereira Barbosa and Fernanda Dreux Miranda\nFernandes",authors:[{id:"28286",title:"Dr.",name:"Fernanda Dreux Miranda",middleName:null,surname:"Fernandes",slug:"fernanda-dreux-miranda-fernandes",fullName:"Fernanda Dreux Miranda Fernandes"},{id:"171244",title:"Dr.",name:"Milene Rossi P.",middleName:null,surname:"Barbosa",slug:"milene-rossi-p.-barbosa",fullName:"Milene Rossi P. Barbosa"}]}],mostDownloadedChaptersLast30Days:[{id:"56698",title:"Risk Factors for Speech-Language Pathologies in Children",slug:"risk-factors-for-speech-language-pathologies-in-children",totalDownloads:1604,totalCrossrefCites:2,totalDimensionsCites:5,abstract:"Risk factors are understood to encompass “aspects of individual behavior or lifestyle, environmental exposure, hereditary or congenital characteristics that are associated with a health related condition”. These are conditions that increase the chances of the child presenting speech-language disorders and that can be avoided, controlled, or treated. Risk is defined as the chance of a child exposed to certain factors (environmental or biological) to acquire or develop speech-language disorders. The objectives of the present study were: to identify the risk factors for speech-language disorders in children up to five years of age and to verify the relationship between risk factors and speech-language diagnostic hypotheses. The aspects of being male gender, prematurity, shyness, being an only child or youngest child, presenting deleterious oral habits, having a family history of speech-language disorders, and use of licit or illicit drugs during pregnancy seem to be the factors that should draw the attention of the health professionals in child development. Therefore, the monitoring of children who have these risk factors should be performed in order to promote the necessary stimulation and the construction of healthy environments.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Daniela Regina Molini-Avejonas, Laís Vignati Ferreira and Cibelle\nAlbuquerque de La Higuera Amato",authors:[{id:"38599",title:"Prof.",name:"Daniela",middleName:null,surname:"Molini-Avejonas",slug:"daniela-molini-avejonas",fullName:"Daniela Molini-Avejonas"},{id:"204612",title:"Prof.",name:"Cibelle",middleName:null,surname:"Amato",slug:"cibelle-amato",fullName:"Cibelle Amato"},{id:"210543",title:"Ms.",name:"Laís",middleName:null,surname:"Ferreira",slug:"lais-ferreira",fullName:"Laís Ferreira"}]},{id:"56385",title:"Formulaic Language: The Building Block of Aphasic Speech",slug:"formulaic-language-the-building-block-of-aphasic-speech",totalDownloads:1865,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Aphasia is a condition that may appear when parts of the brain (Broca’s or Wernicke’s area) responsible for language production and processing are damaged. In most cases, patients have the left side of their brain affected. Thus, formulaic language remains intact in most cases. During speech therapy, this can be a solid base to build on. Formulaic language consists of formulas that are fixed phrases, stereotypes that behave as a single-unit lexical item. They have a significant role in language acquisition and fluent discourse production. These ready-made parts of speech are stored in the long-term memory. Studies suggest that the processing of formulaic language engages right hemisphere areas of the brain. Due to their language impairment, people with aphasia often have a lower quality of life, consequently social and professional integration for them being problematic. The investigation of preserved patterns, such as formulaic language and impairments related to different aspects of discourse, may provide insights both for clinical practice and for cognitive science, therefore, facilitating a more efficient approach to treatment.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Annamária Győrfi",authors:[{id:"200880",title:"Dr.",name:"Annamaria",middleName:null,surname:"Gyorfi",slug:"annamaria-gyorfi",fullName:"Annamaria Gyorfi"}]},{id:"56266",title:"Discourse: Assessment and Therapy",slug:"discourse-assessment-and-therapy",totalDownloads:3107,totalCrossrefCites:7,totalDimensionsCites:9,abstract:"Discourse is essential for interaction and for the expression of ideas, feelings and opinions. Telling personal stories, such as talking about your day or recounting what happened in the playground, is essential for communication and establishing relationships. However, due to their language impairments, people with aphasia (PWA) and children with developmental language disorder (DLD) often have problems with everyday discourse which impact on their lives more widely. While improvement in language skills is supported by speech-language pathology (therapy), it tends to focus on smaller linguistic components, such as single words and sentences. This chapter outlines how speakers construct discourse in everyday situations and focuses on the meanings that people use discourse to convey, as well as the lexical and grammatical resources they use to convey these meanings. Current methods for discourse analysis will be outlined and key developments in narrative discourse production therapy will be reviewed.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Lucy T. Dipper and Madeleine Pritchard",authors:[{id:"201158",title:"Dr.",name:"Lucy",middleName:null,surname:"Dipper",slug:"lucy-dipper",fullName:"Lucy Dipper"},{id:"208542",title:"Dr.",name:"Madeleine",middleName:null,surname:"Pritchard",slug:"madeleine-pritchard",fullName:"Madeleine Pritchard"}]},{id:"56414",title:"Evidence for Speech Sound Disorder (SSD) Assessment",slug:"evidence-for-speech-sound-disorder-ssd-assessment",totalDownloads:1635,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Comprehensive studies on aspects related to the assessment of different biomedical parameters (acoustic and laryngeal signs and oral airflow amplitude), as well as parameters for speech disorders, articulation rate, speech inconsistency, and speech stimulability, are essential for better professional practice and to understand misarticulations in children with speech sound disorders (SSDs). Different equipments that enable noninvasive collection and analysis of data have become more common in speech-language pathology practice. Studies recently conducted by our research group have emphasized the evaluation of auditory-perceptual processing by means of assessments of central auditory processing, electrophysiology of hearing—considering that pure-tone, speech audiometry, and tympanometry are routinely used with children during the diagnostic phase and motor speech production performed by acoustic analysis of speech, electroglottography, aerodynamic measures, and ultrasound tongue imaging. This chapter presents the recent advances observed in studies with Brazilian-Portuguese speakers aiming to improve the assessment of speech sound disorders and to understand better the relationship between the different processing mechanisms involved in speech.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Haydée Fiszbein Wertzner, Danira T. Francisco, Tatiane F. Barrozo\nand Luciana O. Pagan-Neves",authors:[{id:"204570",title:"Prof.",name:"Haydée",middleName:null,surname:"Wertzner",slug:"haydee-wertzner",fullName:"Haydée Wertzner"},{id:"204572",title:"MSc.",name:"Danira",middleName:null,surname:"Francisco",slug:"danira-francisco",fullName:"Danira Francisco"},{id:"204573",title:"MSc.",name:"Tatiane",middleName:null,surname:"Barrozo",slug:"tatiane-barrozo",fullName:"Tatiane Barrozo"},{id:"204574",title:"Dr.",name:"Luciana",middleName:null,surname:"Pagan-Neves",slug:"luciana-pagan-neves",fullName:"Luciana Pagan-Neves"}]},{id:"56042",title:"Cross-Cultural Adaption of the GRBAS and CAPE-V Scales for Portugal and a New Training Programme for Perceptual Voice Evaluation",slug:"cross-cultural-adaption-of-the-grbas-and-cape-v-scales-for-portugal-and-a-new-training-programme-for",totalDownloads:1516,totalCrossrefCites:1,totalDimensionsCites:3,abstract:"Several methods have been proposed for the perceptual evaluation of voice quality, but the GRBAS and Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V) scales are the most widely used and recommended as part of standardised voice evaluation protocols. In this study, cross-cultural adaptation and translation of the GRBAS (the first translation from the original Japanese version) and CAPE-V scales to European Portuguese were carried out following international guidelines. Results from a study of the intra- and inter-rater reliability of the perceptual evaluation of voices with the GRBAS and CAPE-V scales, before and after a training programme, designed according to the most recent American Speech-Language-Hearing Association and Japan Society of Logopedics and Phoniatrics guidelines, are also reported.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Luis M.T. Jesus, Ana Inês Tavares and Andreia Hall",authors:[{id:"202906",title:"Dr.",name:"Luis",middleName:null,surname:"Jesus",slug:"luis-jesus",fullName:"Luis Jesus"},{id:"204680",title:"Mrs.",name:"Ana Inês",middleName:null,surname:"Tavares",slug:"ana-ines-tavares",fullName:"Ana Inês Tavares"},{id:"204681",title:"Dr.",name:"Andreia",middleName:null,surname:"Hall",slug:"andreia-hall",fullName:"Andreia Hall"}]}],onlineFirstChaptersFilter:{topicId:"1244",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:32,numberOfPublishedChapters:318,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:15,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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",coverUrl:"https://cdn.intechopen.com/series/covers/23.jpg",latestPublicationDate:"June 25th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:0,editor:{id:"280770",title:"Dr.",name:"Katherine K.M.",middleName:null,surname:"Stavropoulos",slug:"katherine-k.m.-stavropoulos",fullName:"Katherine K.M. Stavropoulos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRdFuQAK/Profile_Picture_2022-05-24T09:03:48.jpg",biography:"Katherine Stavropoulos received her BA in Psychology from Trinity College, in Connecticut, USA. Dr. Stavropoulos received her Ph.D. in Experimental Psychology from the University of California, San Diego. She completed her postdoctoral work at the Yale Child Study Center with Dr. James McPartland. Dr. Stavropoulos’ doctoral dissertation explored neural correlates of reward anticipation to social versus nonsocial stimuli in children with and without autism spectrum disorders (ASD). She has been a faculty member at the University of California, Riverside in the School of Education since 2016. Her research focuses on translational studies to explore the reward system in ASD, as well as how anxiety contributes to social challenges in ASD. She also investigates how behavioral interventions affect neural activity, behavior, and school performance in children with ASD. She is also involved in the diagnosis of children with ASD and is a licensed clinical psychologist in California. 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He graduated from the Physics Department of the University of Crete and continued his post-graduate studies at the University Paris 7-Denis Diderot (D.E.A. in Didactic of Physics), University Paris 5-René Descartes-Sorbonne (D.E.A. in Science Education) and received his Ph.D. degree at the University Paris 5-René Descartes-Sorbonne (PhD in Science Education). His research interests include science education in early childhood, science teaching and learning, e-learning, the use of ICT in science education, games simulations, and mobile learning. 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She lives in Assisi, Italy.",institutionString:"Research Institute for Neuroscience, Education and Didactics, Patrizio Paoletti Foundation",institution:null},editorTwo:null,editorThree:null}]},overviewPageOFChapters:{paginationCount:5,paginationItems:[{id:"82394",title:"Learning by Doing Active Social Learning",doi:"10.5772/intechopen.105523",signatures:"Anat Raviv",slug:"learning-by-doing-active-social-learning",totalDownloads:2,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Active Learning - Research and Practice",coverURL:"https://cdn.intechopen.com/books/images_new/11481.jpg",subseries:{id:"89",title:"Education"}}},{id:"82310",title:"Knowledge of Intergenerational Contact to Combat Ageism towards Older People",doi:"10.5772/intechopen.105592",signatures:"Alice Nga Lai Kwong",slug:"knowledge-of-intergenerational-contact-to-combat-ageism-towards-older-people",totalDownloads:8,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Social Aspects of Ageing - Selected Challenges, Analyses, and Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11479.jpg",subseries:{id:"90",title:"Human Development"}}},{id:"81993",title:"Emergent Chemistry: Using Visualizations to Develop Abstract Thinking and a Sense of Scale Within the Preschool Setting",doi:"10.5772/intechopen.105216",signatures:"Karina Adbo",slug:"emergent-chemistry-using-visualizations-to-develop-abstract-thinking-and-a-sense-of-scale-within-the",totalDownloads:4,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Active Learning - Research and Practice",coverURL:"https://cdn.intechopen.com/books/images_new/11481.jpg",subseries:{id:"89",title:"Education"}}},{id:"82252",title:"Early Childhood: Enriched Environments and Roles of Caring Adults",doi:"10.5772/intechopen.105157",signatures:"Analía Mignaton",slug:"early-childhood-enriched-environments-and-roles-of-caring-adults",totalDownloads:4,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Active Learning - Research and Practice",coverURL:"https://cdn.intechopen.com/books/images_new/11481.jpg",subseries:{id:"89",title:"Education"}}}]},overviewPagePublishedBooks:{paginationCount:0,paginationItems:[]},openForSubmissionBooks:{},onlineFirstChapters:{},subseriesFiltersForOFChapters:[],publishedBooks:{},subseriesFiltersForPublishedBooks:[],publicationYearFilters:[],authors:{}},subseries:{item:{id:"95",type:"subseries",title:"Urban Planning and Environmental Management",keywords:"Circular economy, Contingency planning and response to disasters, Ecosystem services, Integrated urban water management, Nature-based solutions, Sustainable urban development, Urban green spaces",scope:"