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Immune dysfunction in Alzheimer disease.

Oleg Butovsky1,2, Neta Rosenzweig3, Kilian L Kleemann3,4

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Summary
This summary is machine-generated.

Peripheral immune cells significantly impact Alzheimer disease (AD) brain health. Understanding immune cell roles and inflammation is key to developing new immunomodulatory therapies for AD.

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Area of Science:

  • Neuroimmunology
  • Alzheimer Disease Pathogenesis
  • Peripheral Immune System

Background:

  • Peripheral immune cells are increasingly recognized for their role in brain homeostasis and Alzheimer disease (AD) pathology.
  • Genome-wide association studies link numerous AD risk variants to genes expressed in immune cells, highlighting innate and adaptive immunity's involvement.
  • Neuroimmunology advances show immune cell crosstalk (T cells, B cells, monocytes, macrophages, neutrophils) influences AD hallmarks like amyloid plaques, tau pathology, and neuroinflammation.

Purpose of the Study:

  • To review peripheral immune alterations in Alzheimer disease (AD).
  • To evaluate therapeutic opportunities targeting immune pathways in AD.
  • To identify knowledge gaps, emphasizing the need for human data in translational research.

Main Methods:

  • Review of emerging evidence on peripheral immune cell involvement in AD.
  • Analysis of mechanistic insights into how peripheral inflammation, immune exhaustion, metabolic dysfunction, and epigenetic changes affect neurodegeneration.
  • Evaluation of potential immunomodulatory therapeutic strategies for AD.

Main Results:

  • Chronic peripheral inflammation, immune exhaustion, metabolic dysfunction, and epigenetic reprogramming can worsen neurodegeneration in AD.
  • These factors promote toxic inflammation and impair brain protein clearance.
  • Immune cell crosstalk modulates key AD pathologies, including amyloid and tau.

Conclusions:

  • Peripheral immune alterations are central to Alzheimer disease (AD) pathogenesis.
  • Novel immunomodulatory strategies (e.g., immune checkpoint inhibition, cytokine targeting) show therapeutic promise for AD.
  • Future AD research must prioritize personalized approaches integrating genetic risk, immune profiling, and aging, using human data for translational progress.