Age-related neurodegenerative diseases form a clinically and neuropathologically diverse group that includes common sporadic diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD), both of which also occur in relatively rare early-onset familial forms; purely familial diseases such as Huntington's disease (HD); and “infectious” prion diseases, which are transmissible. That each of these diseases is characterized by abnormal protein deposition in the brain has been documented, although a causal role for deposition in neurodegeneration has not been proven. However, the significance of the fact that abnormal protein deposition is a shared feature of all of these diseases has perhaps been underappreciated. It is the purpose of this Minireview to draw attention to existing evidence that suggests that the mechanism of protein aggregation and deposition may also be shared and to identify corollaries of this hypothesis that suggest experimental tests of its veracity.

The characteristic amyloid plaques of AD and the scrapie-associated fibrils of the prion diseases contain different proteins: the β-amyloid protein (Aβ,∼ 4 kDa) and the prion protein (PrP,∼ 30 kDa), respectively.(