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Basic Science and Pathogenesis.

Avtar Singh Gautam1, Rakesh Kumar Singh1

  • 1National Institute of Pharmaceutical Education and Research, Raebareli, Lucknow, Uttar Pradesh, India.

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

Interleukin-17A (IL-17A) exacerbates Alzheimer's disease (AD) pathology by increasing neuroinflammation, oxidative stress, and AD markers. Targeting IL-17A may offer a therapeutic strategy for AD progression.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Neuroinflammation is a key driver of Alzheimer's disease (AD) pathology.
  • Interleukin-17A (IL-17A), a pro-inflammatory cytokine, is increasingly linked to AD progression.
  • IL-17A amplifies neuroinflammation, contributing to cellular injury in AD.

Purpose of the Study:

  • To investigate the role of IL-17A in exacerbating amyloid-beta (Aβ)-induced AD pathology.
  • To understand how IL-17A influences key molecular and cellular markers of AD.

Main Methods:

  • AD pathology was induced in mice via intranasal administration of Aβ and recombinant mouse IL-17A (rmIL-17).
  • Different doses of rmIL-17 (1, 2, 4 µg/kg) were administered over seven alternate days.
  • Hippocampal and cortical tissues were analyzed for inflammatory markers, oxidative stress, AD structural markers, and glial cell activation.

Main Results:

  • Co-administration of rmIL-17 with Aβ intensified IL-17A signaling, increased pro-inflammatory cytokines, and elevated oxidative stress.
  • Antioxidant levels were reduced, while key AD markers (pTau, Aβ, BACE1) were upregulated.
  • Astrocytes and microglia were activated, with microglia shifting to a pro-inflammatory phenotype.

Conclusions:

  • IL-17A significantly aggravates AD pathology.
  • IL-17A emerges as a potential therapeutic target for managing Alzheimer's disease progression.