Aging, the brain and human prion disease.

Human prion diseases (PrD) preferentially manifest in the elderly. Their neuropathology may coexist with tau immunoreactive neuropil threads, neurofibrillary tangles, and beta-amyloid senile plaques, most likely representing an age-related change rather than a pathogenic link with Alzheimer's disease. Cerebrovascular disease with brain infarction, another malady preferring the elderly, is useful to prove the origin of PrD-associated prion protein deposition exclusively from neurons.