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The brain suffers cellular aging with advancing age. Because of incremental damage to cellular organelles and chromatin and because of the aging and decrement of function of other organ systems (e.g., cardiovascular causes result in multi-focal injury to white matter in most individuals, as assayed by MRI, in the eighth decade of life). Studies of neuron numbers in different cell groups in the brain indicate that there is normally a slow loss of cells with aging, and a compensatory extension and increase in the complexity of the branching of remaining neurons. As a result, with aging there is some loss of plasticity of brain responsiveness.
More rapid and serious loss of cognitive function may be superimposed upon this picture of normal aging. When the loss is acute or subacute, it is due to a metabolic encephalopathy, such as an electrolyte abnormality or hepatic failure, or drug toxicity. When the loss of function occurs in one or more discrete episodes, it is more likely to be due to multiple cerebral infarcts, which is still a common cause of dementia (about 15-20 % of cases). However, as we have learned to control the risk factors for stroke (especially blood pressure and diabetes) and to treat a variety of metabolic disorders, a population has emerged in the latter half of this century of elderly people who lose mental function slowly, progressively, and inexorably over a period of months to years. Only a few treatable medical conditions present in this way (thyroid disease, vitamin B1 or B12 deficiency, subdural hematomas, hydrocephalus, or rarely syphilis or another cause of chronic meningitis or encephalitis), and the workup of a patient with dementia largely consists of eliminating these potentially treatable disorders. Once these conditions have been eliminated, the remaining group, who account for 80-45 % of the demented elderly, are found to have a degenerative neurological cause aging,
Alzheimer's disease is the aging disease best known of the degenerative causes of dementia, and it accounts for about 80-90% of this group. Alzheimer's disease is an enormous problem medically and economically, affecting about 5 % of those between the ages of 65-70, and increasing in percentage with increasing age. As many as 20 % of individuals over 80 were affected, with a lifetime occurrence of 40% of individuals who live to this age range. Recent studies examining the relationship of the presence of the apolipoprotein indicate that nearly all individuals with E4/E4 genotype will eventually develop
The damage to the brain in Alzheimer's disease is caused by the Aging Alzheimer's disease Alzheimer Aricept Dementia deposition of two types of pathological changes in the brain. First, there is deposition of ß-amyloid protein which forms extracellular plaques. The ß-amyloid protein causes local tissue injury, but is not aging, many normal elderly individuals have enormous ß-amyloid protein burdens, with very little change in mental function.
However, ß-amyloid protein appears to induce a second pathological change, neurofibrillary degeneration. It is not known why neurofibrillary pathology develops in some individuals with ß-amyloid protein deposition, and not in others. However, the affected neurons accumulate fibrils which are composed of paired, helical filaments. The paired, helical filaments are, in turn, composed of a hyper-phosphorylated form of the tau protein.
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