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Alzheimer's disease: new light on etiology and management.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder of the central nervous system leading to the most common form of age-associated dementia. More than a century has passed since 1907 when Alois Alzheimer first described the neuropathological hallmarks of the dementia that now bears his name. During this time, our understanding of the biological, environmental, and genetic factors that drive this disorder followed progress in the fields of molecular biology, neuroscience, and genetics. It could be said that the modern era of understanding the biological factors involved in AD started in the early 1980s with the first efforts to elucidate the molecular nature of the neuropathological markers found in the brains of affected individuals. These markers include neuritic amyloid plaques, neurofibrillary tangles, and cerebrovascular amyloidosis. Interestingly, a volume on a symposium on amyloid and amyloidosis held in 1979 makes no reference to the amyloidosis of AD,1 and this indicates that even at this late date, there was little effort directed at the neuropathology of AD. Neuritic amyloid plaques are complex extracellular structures containing at their core amyloid deposits of fibrillar amyloid beta (Aβ) protein surrounded by reactive astrocytes, microglia, and dystrophic neurites. In contrast to the extracellular localization