Abstract

Progressive mental deterioration in old age has been recognized and described throughout human history. However, it was not until the early part of the 20th century that a specific neuropathologic change, the neurofibrillary tangle, was identified by Alois Alzheimer in 1906. Alzheimer identified this change at autopsy in the cerebral cortex of a relatively young patient suffering from progressive cognitive decline. Also present were collections of amorphous debris, previously known as ‘miliary foci’ or ‘nodules of neurosclerosis’ and now known as the senile plaque, although these were described in years prior and associated with so-called dementia senilis. Nevertheless, the atypical clinical presentation, especially the young age at onset, justified a new disease, Alzheimer disease (AD). The definition over time was separated into Alzheimer's disease, or the presenile form, and senile dementia of the Alzheimer-type, based on an arbitrary age cut-off of 65. Although these classifications are still sometimes referred to, AD fails to demonstrate either a bimodal age of onset or phenotypic differences. AD is now viewed as a single entity with a prevalence that increases sharply with age. Indeed, 10% of the population older than 65 years and as many as 47% of those older than 85 years may be affected. Prevalence studies project that 114 million people will be affected worldwide by 2050, and 13.2 million of these will be in the United States.

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