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Alzheimer’s disease (AD), already one of the most serious health problems in the U.S., will carry an ever burgeoning impact as the proportion of elderly continues to increase. Clinically, AD is a progressive neurodegenerative disorder characterized by global cognitive decline. Neuropathologically, the brains of AD patients contain abundant amounts of neurofibrillary tangles (NFT) and β-amyloid in the form of senile plaques (SP) and blood vessel deposits. While the etiological events that lead to AD have not been clearly resolved, genetic factors clearly play a major role; there is an emerging consensus that AD is a complex and genetically heterogeneous disorder that is best explained by an age-dependent dichotomous model. On one hand, early-onset (<60) AD is caused by defects in any of three different genes: presenilin 1 (PSEN1) on chromosome 14 (1), presenilin 2 (PSEN2) on chromosome 1 (2), and the amyloid β protein precursor (APP) on chromosome 21 (3). On the other hand, late-onset AD is associated with genetic polymorphisms that appear to operate as risk factors and/or genetic modifiers.

A genetic dichotomy model for the inheritance of Alzheimer’s disease and common age-related disorders