Alzheimer’s disease

progressive mental deterioration manifested by loss of memory, ability to calculate, and visual-spatial orientation; confusion; disorientation. Begins in late middle life and results in death in 5–10 years. Pathologically, the brain is atrophic, especially in the frontal occipital and temporal regions; histologically, there is distortion of the intracellular neurofibrils (neurofibrillary tangles) and senile plaques composed of granular or filamentous argentophilic masses with an amyloid core, found predominantly in the cerebral cortex, amygdala, and hippocampus; the cerebral cortex has few and shrunken neurons which may contain cytoplasmic vacuoles and argentophilic granules displacing the nucleus to the periphery; the most common degenerative brain disorder. Syn: Alzheimer’s dementia, presenile dementia(2), dementia presenilis, primary neuronal degeneration, primary senile dementia.

Alzheimer’s accounts for some 60–70% of senile dementias, which in the U.S. afflict 5–10% of those over age 65, and 20% of those over age 80. In recent years, clinicians have instituted a protocol for monitoring the progress of the disease, known as FAST (functional assessment stages). Basic understanding of the brain changes brought about by Alzheimer’s has been greatly aided by MRI and PET scanning; however, the cause of the disease is not yet clear. Arguments have been advanced for genetic, environmental, viral, neurochemical, and immunological causes. With the aging of the post-WW2 generation, the ranks of Alzheimer’s patients are expected to swell, making the need for adequate diagnostic techniques and therapies more pressing. Treatments being explored include drugs to correct neurochemical imbalances. Some researchers are investigating repairing or augmenting damaged nerves through application of nerve growth factor or neural tissue transplants, but this approach remains highly experimental.