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Basic Science and Pathogenesis.

Nicolas Gabriel Gonzalez Perez1,2, Carlos Javier Pomilio1,2, Luciano Arcucci1,2

  • 1CONICET, Buenos Aires, Argentina.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Summary
This summary is machine-generated.

Metformin (MET) treatment improved cognitive function and reduced amyloid pathology in Alzheimer's Disease (AD) mouse models. This therapeutic effect is linked to restored microglial autophagic flux, suggesting MET's potential for AD treatment.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • Alzheimer's Disease (AD) and type 2 diabetes mellitus (T2D) share neuroinflammation and impaired autophagy.
  • Metformin (MET), a T2D drug, reduces microglial activation and improves autophagy in T2D models.

Purpose of the Study:

  • Evaluate metformin's therapeutic potential for experimental Alzheimer's Disease.
  • Investigate metformin's effects on neuroinflammation, amyloid pathology, and cognitive function in AD models.

Main Methods:

  • Treated PDAPP-J20 mice with metformin or vehicle, assessing spatial memory, amyloid pathology, neurogenesis (DCX), and microglial status.
  • In vitro: Exposed BV2 microglial cells to amyloid-beta (Aβ) peptides and metformin, evaluating autophagic flux.

Main Results:

  • Metformin improved spatial memory, hippocampal neurogenesis, and reduced amyloid pathology in AD mice.
  • Metformin reversed decreased TMEM119 expression and restored microglial autophagic flux (reduced p62).
  • In vitro, metformin reversed Aβ-induced autophagic flux blockade in microglial cells.

Conclusions:

  • Metformin demonstrates therapeutic potential in AD models by restoring cognitive performance.
  • The mechanism involves microglial functional recovery via rehabilitation of amyloid-blocked autophagic flux.
  • Metformin may also reduce amyloid pathology and enhance hippocampal neurogenesis.