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Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response.

Anna A Pimenova1, Manon Herbinet2, Ishaan Gupta3

  • 1Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Ronald M. Loeb Center for Alzheimer's disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Neurobiology of Disease
|December 10, 2020
PubMed
Summary

The master regulator SPI1/PU.1 influences Alzheimer's disease (AD) risk. Higher PU.1 expression increases inflammation and AD risk, while lower expression is protective by reducing inflammation and promoting cell death.

Keywords:
Alzheimer's diseaseAmyloid βAnti-inflammatory microgliaDisease-associated microgliaPU.1Phagocytosis

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) has over forty genetic risk loci, many enriched in myeloid cell enhancers.
  • Microglia, the brain's immune cells, are implicated in AD pathogenesis.
  • SPI1/PU.1, a key regulator of myeloid development, is a genetic risk factor for AD.

Purpose of the Study:

  • To investigate the molecular and cellular effects of altered SPI1/PU.1 expression in microglia.
  • To understand how PU.1 levels impact microglial function and AD risk.

Main Methods:

  • Stable overexpression and knockdown of PU.1 in the BV2 microglial cell line.
  • Transcriptome analysis to assess gene expression changes.
  • Assessment of phagocytic activity and cellular responses to cytotoxic conditions.

Main Results:

  • Reduced PU.1 suppressed homeostatic genes and activated antioxidant and lipid metabolism pathways, decreasing pro-inflammatory gene expression.
  • PU.1 knockdown decreased phagocytic uptake but retained myelin internalization.
  • Altered PU.1 levels modulated microglial responses, including pro-inflammatory signaling and cell viability.

Conclusions:

  • Increased SPI1/PU.1 expression may drive AD risk through enhanced pro-inflammatory responses and cell viability.
  • Lower SPI1/PU.1 expression may be protective by increasing cell death and reducing inflammation, potentially mitigating A1 reactive astrocyte signatures.