TL;DR
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.
This work situates MiET formation within the broader microglial functional repertoire and focuses on how ET-dominant responses may compromise homeostatic or neuroprotective roles, expanding the conceptual framework for microglial pathogenicity and inviting future mechanistic and translational research.
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.
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...
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.
A “cellular state–pathological network–therapeutic window” framework is proposed and the roles of microglia in amyloid-β plaque seeding and compaction, NLRP3 inflammasome activation, mitochondrial DNA–cGAS–STING signaling, complement-mediated synaptic engulfment, and bidirectional microglia–tau feedback are systematica...
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β accumulation, tau pathology, synaptic failure, neurovascular dysfunction, mitochondrial injury and chronic neuroinflammation. While amyloid and tau remain central pathological features, the inflammatory state of the brain is...
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