Figure 2
From: Examining the mechanisms that link β-amyloid and α-synuclein pathologies
Potential mechanisms linking β-amyloid and α-synuclein pathology. Studies support several putative mechanisms by which β-amyloid (Aβ) and α-synuclein (α-syn) may interact to enhanced pathology and cognitive decline. Such mechanisms include (left to right): chronic inflammation and microglial activation induced by both Aβ and α-syn; direct interactions and hybrid oligomerization of Aβ and α-syn; Aβ-induced kinase activation and α-syn phosphorylation; impairment of proteasome and autophagy degradation pathways; and Aβ-induced phosphorylation of tau leading to tau-mediated enhancement of α-syn aggregation. CK-2, casein kinase 2; PLK-2, polo-like kinase 2; PHF, paired helical filaments; NFT, neurofibrillary tangle; p-Tau, phosphorylated tau; pS129, phosphorylated at serine 129; p-syn, phosphorylated α-synuclein; UPS, ubiquitin-proteasome system.