Fig. 9From: Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits in a mouse model of DLB/PDSchematic depiction of the potential microglial networks and pathways that interact in aging and synucleinopathies. The effects of aging processes and extracellular ɑ-syn convergence in the macrophages/microglia in the CNS probably by engaging both Toll-like receptors (TLRs) such as TLR2 and colony stimulating factor receptors (CSF-R) that in turn activate pro-inflammatory LPS-like pathways with increased production of cytokines including TNFɑ, IL6, IL10ɑ and activation of networks involving CSF2. This in turn results in a cascade of events involving further activation of microglia, astrocytes and trafficking of T cells into the CNS parenchyma that jointly produce pro-inflammatory neurotoxic factors leading to neurodegenerationBack to article page