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Basic Science and Pathogenesis.

Kirstin A Tamucci1, Badri N Vardarajan2, Elizabeth M Bradshaw3

  • 1Columbia University, New York, NY, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
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Summary
This summary is machine-generated.

Alzheimer's disease risk gene CD33 influences microglial metabolism. Genetic variations in CD33 alter cellular energy production and reveal a novel interaction with GLUT1, impacting AD pathogenesis.

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Area of Science:

  • Neuroimmunology
  • Metabolic pathways in neurodegeneration
  • Alzheimer's disease genetics

Background:

  • The innate immune system, particularly microglia, plays a crucial role in Alzheimer's disease (AD) pathogenesis.
  • Over 75% of AD genetic loci are linked to innate immune genes, with CD33 being a significant AD risk gene.
  • CD33, expressed by microglia, is known to modulate inflammatory responses and microglial metabolism, but the precise impact of its genetic variations remains unclear.

Purpose of the Study:

  • To investigate how CD33 genetic variations influence microglial metabolism and energy production.
  • To elucidate the mechanisms by which CD33 affects microglial bioenergetics in the context of AD.
  • To identify potential molecular interactions underlying CD33's role in AD pathogenesis.

Main Methods:

  • Generation of human microglia-like cells from monocytes with distinct CD33 genotypes.
  • Measurement of cellular respiratory bioenergetics and metabolic profiles.
  • Mass spectrometry, proximity ligation assay (PLA), and co-immunoprecipitation (co-IP) to identify CD33 binding partners.
  • Analysis of ROSMAP cohort RNA sequencing data to assess CD33:GLUT1 interaction in AD.

Main Results:

  • Significant variations in ATP production via oxidative phosphorylation and glycolysis were observed based on CD33 genotype.
  • AD-protective CD33 genotypes exhibited higher glycolytic activity and lower glucose uptake, linked to increased hexokinase activity.
  • A novel interaction between CD33 and the glucose transporter GLUT1 was identified, validated in human cell lines and associated with AD in patient data.

Conclusions:

  • Genetic variations in the AD-associated gene CD33 induce specific metabolic alterations in microglia.
  • The newly discovered CD33:GLUT1 interaction represents a critical link between genetic, immune, and metabolic factors in AD.
  • This research opens avenues for novel therapeutic and immunomodulatory strategies targeting microglial metabolism to combat Alzheimer's disease.