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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Amy F Lloyd1

  • 1University of Dundee, Dundee, Angus, United Kingdom.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Microglia utilize internal glycogen stores to fuel inflammatory responses in Alzheimer's Disease (AD). Targeting glycogen metabolism may offer a novel therapeutic strategy for neurodegenerative diseases.

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Area of Science:

  • Neuroimmunology
  • Metabolic pathways in neurodegeneration
  • Alzheimer's Disease pathogenesis

Background:

  • Chronic inflammatory microglia are central to Alzheimer's Disease (AD) pathology, exhibiting high metabolic demands.
  • Sustained hyperglycemia is a known risk factor for AD, highlighting the critical role of glucose metabolism.
  • Understanding microglia metabolic fueling is crucial for developing therapeutic strategies in neurodegenerative diseases.

Purpose of the Study:

  • To investigate the metabolic pathways utilized by microglia during Alzheimer's Disease progression.
  • To determine the role of glucose and glycogen in microglia inflammatory responses.

Main Methods:

  • Microglia were isolated from APP-NL-G-F mice at 1, 3, and 6 months of disease progression.
  • Proteomic analysis and mass spectrometry were employed to interrogate microglia.
  • In vitro glucose depletion experiments were conducted to assess microglia inflammatory responses.

Main Results:

  • Microglia significantly upregulated glycolysis and inflammatory protein expression at 6 months.
  • Glucose receptor expression decreased, while glycogen breakdown proteins increased.
  • Microglia relied on glycogen reserves for metabolic flexibility and inflammatory responses, with prolonged glucose depletion altering their function.

Conclusions:

  • Microglia use internal glycogen stores to fuel inflammatory responses to amyloid and LPS.
  • Glycogen-modulated microglia responses present a potential therapeutic target for neuroinflammation in neurodegenerative diseases.