The protein α-synuclein, like amyloid-β and tau, forms into an increasing amount of solid aggregates in the aging brain. These aggregates and their surrounding biochemistry cause neural dysfunction and cell death. Every older individual has raised levels of these protein aggregates, and the pathology they cause rises to the level of named condition when one or another is present in great enough amounts. The age-related diseases associated with α-synuclein are termed synucleinopathies, though one can argue that all neurodegeneration is to some degree influenced by all protein aggregates. Where the research, medical, and regulatory communities choose to draw the line between “normal” and “pathological” is somewhat arbitrary. If methods of reliably removing protein aggregates existed, every older individual should undergo treatment on a periodic basis, not just people with notably high levels of aggregates.
Parkinson’s disease is the best known of the synucleinopathies, alongside dementia with Lewy bodies, and a few other less common conditions. Arguably α-synuclein is a meaningful cause of pathology in Alzheimer’s patients as well. It might be better to think of the named conditions as rough, shifting territories outlined on a broad map of brain aging that combines differing levels of protein aggregation, vascular dysfunction, mitochondrial aging,
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