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Encephalitis ll: Pathophysiology01:26

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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Related Experiment Video

Updated: Apr 23, 2026

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
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Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

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Microglial pathology.

Wolfgang J Streit, Qing-Shan Xue, Jasmin Tischer

    Acta Neuropathologica Communications
    |September 27, 2014
    PubMed
    Summary
    This summary is machine-generated.

    Aging brains show both inflammation and senescence in microglial cells, the brain's immune cells. This dual decline, driven by free radical damage, impairs immune function and impacts cognition in aging and Alzheimer's disease.

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    Area of Science:

    • Neuroscience
    • Immunology
    • Pathology

    Background:

    • Microglial cells are key immune cells in the brain.
    • Aging and neurodegenerative diseases like Alzheimer's disease (AD) involve microglial changes.
    • Conflicting evidence exists regarding whether microglia become hyperactive (neuroinflammation) or weakened (senescence) with age.

    Purpose of the Study:

    • To summarize microglial pathological changes in human aging and AD.
    • To compare human and rodent microglial changes during aging and disease.
    • To reconcile the concepts of neuroinflammation and microglial senescence in aging and AD.

    Main Methods:

    • Review of pathological changes in human and animal models.
    • Comparison of microglial alterations in humans versus rodents.
    • Analysis of the impact of aging-associated free radical injury on microglia.

    Main Results:

    • Microglial cells exhibit both senescence (dystrophic changes) and low-grade neuroinflammation during aging and AD.
    • Both processes stem from aging-associated free radical injury.
    • These combined effects exhaust microglia, leading to an impaired brain immune system.

    Conclusions:

    • Microglial senescence and neuroinflammation are not contradictory but are synergistic consequences of aging.
    • This synergistic damage weakens the brain's immune system, compromising neuronal function and cognition.
    • Understanding these dual microglial pathologies is crucial for addressing aging-related cognitive decline and AD pathogenesis.