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Alzheimer's Disease: Overview01:26

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
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Systemic Inflammation Causes Microglial Dysfunction With a Vascular AD phenotype.

Praveen Bathini1, Isabel Dupanloup2, Elena Zenaro3

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Brain, Behavior, & Immunity - Health
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Systemic inflammation in early life, triggered by PolyI:C, leads to progressive neuroinflammation and tauopathy in mice, mirroring aspects of Alzheimer's and vascular dementia. This highlights the critical role of early immune insults in neurodegenerative disease development.

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Systemic inflammation, originating outside the central nervous system (CNS), impacts brain health and is linked to neurodevelopmental and neurodegenerative disorders.
  • Chronic inflammation from infections or stress may contribute to dementia, including Alzheimer's disease (AD) and vascular dementia (VaD).
  • Early life immune insults can trigger neuroinflammatory cascades, altering brain gene expression and contributing to pathologies seen in AD and VaD.

Purpose of the Study:

  • To investigate the long-term pathological effects of systemic inflammation induced by Polyinosinic:polycytidylic acid (PolyI:C) in a mouse model.
  • To compare the temporal evolution of hippocampal transcriptomic changes in PolyI:C-exposed mice with human post-mortem brain specimens from AD and VaD patients.
  • To assess the impact of chronic low-grade systemic inflammation on neuroinflammation, tauopathy, and microglial changes.

Main Methods:

  • Developed a PolyI:C sterile infection model in C57BL6 mice to induce chronic low-grade systemic inflammation.
  • Conducted a cross-sectional analysis of aging mice (3-16 months) exposed to PolyI:C or saline (control).
  • Compared hippocampal brain aging phenotypes with human post-mortem brain samples from mild AD, severe AD, and Vascular Dementia (VaD) patients.

Main Results:

  • PolyI:C mice exhibited peak peripheral and central inflammation at 6 months, accompanied by memory deficits.
  • Progressive tauopathy was observed in the hippocampus, with microglia showing aging-dependent shifts towards a phagocytic phenotype.
  • Transcriptomic analysis revealed significant gene expression changes throughout aging, peaking at 9 months, with upregulation of the proinflammatory marker Lcn2.
  • Validation in human AD and VaD brains showed reproducibility of some gene targets, particularly in VaD specimens.

Conclusions:

  • The PolyI:C model demonstrates that chronic peripheral inflammation induces progressive tau hyperphosphorylation, microglial changes, and astrogliosis.
  • Gene reprogramming in PolyI:C mice reflects increased neuroinflammation, vascular remodeling, and neuronal dysfunction, similar to human AD and VaD.
  • These findings suggest that early-life immune insults play a crucial role in the development of neurodegenerative diseases.