Alzheimer’s disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer’s disease (AD) are extracellular Amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with Aβ plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modifying therapies for AD that are currently being studied in phase I–III trials.
Part of the book: Geriatric Medicine and Gerontology
Nonconvulsive status epilepticus (NCSE) is common in patients with coma with a prevalence between 5 and 48%. Nonconvulsive status epilepticus (NCSE) is an electroclinical state associated with an altered mental status (AMS) but lacking convulsive motor activity. It is difficult to diagnose in the obtunded/comatose patients. Such patients have often other serious medical conditions, and the diagnosis of NCSE is frequently delayed in these patients. Diagnosing NCSE demands a high degree of clinical suspicion and for that reason likely remains under-recognized. The most important question, however, is whether the treatment of NCSE in coma improves the outcome of these patients or not. In this review, we aimed to summarize the EEG patterns in NCSE to further delineate the borders between comatose forms of NCSE and coma-epileptiform discharges and to evaluate modified EEG criteria for NCSE in a coma.
Part of the book: Disorders of Consciousness
Alzheimer’s disease (AD) is a neurodegenerative disorder that accounts for nearly 70% of the more than 50 million dementia cases estimated worldwide. There is no cure for AD. Currently, AD diagnosis is carried out using neuropsychological tests, neuroimaging scans, and laboratory tests. In the early stages of AD, brain computed tomography (CT) and magnetic resonance imaging (MRI) findings may be normal, but in late periods, diffuse cortical atrophy can be detected more prominently in the temporal and frontal regions. Electroencephalogram (EEG) is a test that records the electrical signals of the brain by using electrodes that directly reflects cortical neuronal functioning. In addition, EEG is noninvasive and widely available at low cost, has high resolution, and provides access to neuronal signals, unlike functional MR or PET which indirectly detects metabolic signals. Accurate, specific, and cost-effective biomarkers are needed to track the early diagnosis, progression, and treatment response of AD. The findings of EEG in AD are now identified as biomarkers. In this chapter, we reviewed studies that used EEG or event-related potential (ERP) indices as a biomarker of AD.
Part of the book: Neurodegenerative Diseases