Alpha-synuclein biology Neuroinflammation
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Co-pathology proteins (tau, amyloid-β, TDP-43) and alpha-synuclein share neuroinflammatory mechanisms that create a feed-forward cycle accelerating aggregate formation and neurodegeneration across all protein types.
Oligomeric species of tau, amyloid-β, and alpha-synuclein each elicit inflammatory responses from microglia and astrocytes; the resulting proinflammatory environment in turn promotes further aggregation of all pathological proteins, so co-pathology burden and neuroinflammation severity amplify each other.