TL;DR
This network is interconnected, and understanding it is crucial in the creation of therapies that attempt to restore proteostasis, inhibit inflammation, and increase neurotrophic signalling to delay or prevent PD progression.
It is proposed that the α-synuclein pathology starts in the gut with the non-motor symptoms, and then it propagates to the brain via the vagus nerve causing motor symptoms, which has emerged as an attractive target for immunotherapies.
Advanced fluid biomarkers, such as seed amplification assays (SAA), alongside multidimensional neuroimaging techniques (PET, SPECT, MRI), are proving crucial for detecting these early microglial and pathological changes to guide personalized, disease-modifying therapies of PD.
An integrative model in which neuroinflammation and metabolic dysfunction function not merely in parallel, but as mutually reinforcing components of a self-amplifying pathological circuit is proposed, while acknowledging that this model remains to be fully validated and that alternative causal architectures are possibl...
It is suggested that microglia-mediated ECM remodeling serves as a mechanistic link between neuroinflammation and neuronal susceptibility in PD.
Alzheimer's disease (AD) is a progressively debilitating neurodegenerative condition characterized by the accumulation of amyloid-β (Aβ), tau pathology, synaptopathy, and neuron loss. Recent studies suggest that Neuroinflammation is a critical part of the disease process rather than an accompanying feature of the menti...
This review systematically summarizes current research on astrocyte involvement in PD pathology and their neuronal interaction mechanisms, further exploring their interconnections to elucidate disease pathogenesis.
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