ABSTRACT
Parkinson’s disease (PD) and Alzheimer’s disease (AD) may be pathogenically linked by a single common mechanism: the aggregation and deposition of misfolded proteins (1-3). Indeed, as summarized in Table 1, nearly every major neurodegenerative disease is pathologically characterized by the insidious accumulation of insoluble filamentous aggregates of normally soluble proteins in the central nervous system (CNS) (3). Since these filamentous aggregates show the ultrastructural and tinctorial properties of amyloid (i.e., ~10 nm wide fibrils with crossedβ-pleated sheet structures that stain with congo red, thioflavin-S, or other related dyes), these diseases are appropriately linked together as brain amyloidoses (4). An understanding that PD and other neurodegenerative parkinsonian diseases including cortical basal degeneration (CBD), progressive supranuclear palsy (PSP), and frontal temporal dementia with parkinsonism linked to chromosome 17 (FTDP17) are related brain amyloidoses may permit novel insights into the pathogenesis of these common movement disorders and ultimately may lead to improvements in diagnosis and therapy for these devastating diseases.
