This review critically examines glial-centered hypotheses of neurodegeneration, with emphasis on their roles in early disease phases.
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glial-centered hypotheses of neurodegeneration
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A self-amplifying astrocyte-microglia-neuron inflammatory feedback loop is implicated in early neurodegeneration.
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a self-amplifying astrocyte-microglia-neuron inflammatory feedback loop
Astrocytic scar formation in neurodegeneration is driven by AQP4, MMP-9, GFAP/vimentin, connexins, and JAK/STAT3 signaling.
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astrocytic scar formation driven by aquaporin-4 (AQP4), matrix metalloproteinase-9 (MMP-9), glial fibrillary acidic protein (GFAP)/vimentin, connexins, and janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling
Early neurodegeneration involves microglial polarization from an M2 neuroprotective state to an M1 proinflammatory state.
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microglial polarization from an M2 neuroprotective state to an M1 proinflammatory state
Impaired microglial phagocytosis and extracellular-vesicle-mediated propagation of beta-amyloid and tau are implicated in early neurodegeneration.
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impaired microglial phagocytosis and extracellular-vesicle-mediated propagation of β-amyloid (Aβ) and tau
NLRP3 inflammasome assembly occurs via P2X7R-mediated potassium efflux in the glial-centered pathogenesis framework discussed by the review.
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NLRP3 inflammasome assembly via P2X purinergic receptor 7 (P2X7R)-mediated K+ efflux
Glial dysfunction arises during the earliest stages of neurodegeneration, precedes overt neuronal loss, and may act as a primary driver of disease onset.
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many of these phenotypic transitions arise during the earliest stages of neurodegeneration, when glial dysfunction precedes overt neuronal loss and may act as a primary driver of disease onset
A comprehensive multitargeted approach is essential for mitigating Alzheimer's disease and related neurodegenerative disorders because glial phenotypes and molecular isoforms are complex.
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Given the complexity of glial phenotypes and molecular isoform diversity, a comprehensive, multitargeted approach is essential for mitigating Alzheimer's disease and related neurodegenerative disorders.
Interventions that restore neuroglial homeostasis at the earliest stages of disease may have the greatest potential to delay or prevent progression.
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Interventions that restore neuroglial homeostasis at the earliest stages of disease may hold the greatest potential to delay or prevent progression.
Promising therapeutic strategies focus on normalizing glial phenotypes rather than simply suppressing pathology.
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Promising therapeutic strategies target ... with a focus on normalizing glial phenotypes rather than simply suppressing pathology.