Alzheimer's disease overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
|
Alzheimer's disease Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Alzheimer's disease overview On the Web |
|
American Roentgen Ray Society Images of Alzheimer's disease overview |
|
Risk calculators and risk factors for Alzheimer's disease overview |
Overview
Alzheimer's disease is the most common cause of dementia among older people. Dementia is a loss of thinking, remembering, and reasoning skills that interferes with a person's daily life and activities. Other causes of dementia include blood vessel disease in the brain (called vascular dementia), Parkinson's disease, frontotemporal dementia, and Lewy body dementia.
Historical Perspective
The first case of Alzheimer's disease was described by a German psychiatrist named Alöis Alzheimer in the year 1901. For many decades after Alzheimer's original description, there was little progress in defining the pathogenesis of AD occurred. In the mid 1970's, it was found that the levels of acetylcholine decrease in brains of individuals undergoing neurodegeneration due to Alzheimer's disease. In early 1980's major advances in biochemistry and molecular genetics allowed the use of compositional analyses and immunocytochemistry to explain the structure of tangles and plaques found in the brains of Alzheimer patients. The term Alzheimer's disease was subsequently formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.
Classification
Alzheimer's disease may be classified according to severity into mild, moderate and severe dementia. It may also be classified based on age of onset into early onset and late onset Alzheimer's disease. Another method of classification of Alzheimer's disease is based on the course of disease into pre-dementia, early dementia, moderate dementia and advanced dementia.
Pathophysiology
Alzheimer disease (AD), is a progressive neurodegenerative disorder. The dysfunction of amyloid precursor protien (APP) metabolism and the resulting build up of of Aβ peptides and their aggregation in the form of senile plaques in the brain parenchyma of individuals have been considered pivotal for neurodegeneration in the disease. Cognitive impairment in patients with AD is closely associated with synaptic loss in the neocortex and limbic system. In familial forms of AD, mutations result in an increased Aβ production or aggregation, in sporadic AD, failure of the clearance mechanisms might play a key role. Loss of mature neurons and alterations in neural progenitor cells (NPCs) in areas such as the dentate gyrus (DG) of the hippocampus have been found to be responsible for manifestations of AD. On gross pathology, temporal atrophy (hippocampus in particular), dilation of lateral ventricles and third ventricle are characteristic findings of Alzheimer's disease. The microscopic histopathological features of alzheimer's disease consist neurofibrillary tangles, senile plaques, neuronal loss, and with or without cerebral amyloid angiopathy.