Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication - PubMed

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Alzheimer's disease (AD) research is shifting from an amyloid-beta (Aβ) focus to a neuroimmune network perspective.
Microglial and astrocytic dysfunctions are key contributors to AD progression, with disease-associated microglia (DAM) showing reduced Aβ clearance and increased pro-inflammatory factor release.
Astrocytes lose homeostatic support functions and gain neurotoxic properties in AD.
Intercellular communication molecules, including cytokine/chemokine networks, extracellular vesicles (EVs), and the complement system, play pivotal roles in disease progression.
Peripheral immune cell infiltration and gut-brain axis dysregulation expand the pathological scope of AD.
Therapeutic strategies are evolving towards multi-target interventions, such as immune modulation, exosome-based drug delivery, and combination therapies.
Future directions include addressing disease heterogeneity and developing personalized treatments, with early interventions targeting intercellular communication offering new hope.

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