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Related Experiment Video

Updated: Jan 7, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Xuelin Gu1, Tim Distel1, Konrad Talbot1

  • 1Loma Linda University, Loma Linda, CA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary

Brain insulin resistance, marked by elevated IRS-1 pS616, increases with age and peaks in Alzheimer's disease dementia (ADd). This pathology correlates with AD hallmarks, suggesting a role in disease development and potential as a therapeutic biomarker.

Area of Science:

  • Neuroscience
  • Pathology
  • Biomarker Discovery

Background:

  • Alzheimer's disease (AD) pathogenesis involves beta-amyloid and tau, with brain insulin resistance also a common feature.
  • Elevated insulin receptor substrate-1 phosphorylated at serine-616 (IRS-1 pS616) is found in AD dementia (ADd) neurons.
  • Semaglutide, an antidiabetic, is in clinical trials for AD, highlighting the therapeutic potential of targeting insulin resistance.

Purpose of the Study:

  • To quantify IRS-1 pS616 in hippocampal neurons of normal and ADd cases.
  • To investigate correlations between IRS-1 pS616, AD pathologies, and subject demographics.
  • To explore IRS-1 pS616 as a potential biomarker for brain insulin resistance in AD.

Main Methods:

  • Immunohistochemistry on hippocampal sections from 217 age- and sex-matched cases (NCI, preclinical, MCI, ADd).

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  • Quantification of beta-amyloid, phospho-tau, and IRS-1 pS616 using AI-based digital pathology (U-Net neural networks).
  • Analysis of correlations between pathologies, age, and ApoE genotype.

    • Main Results:

    • IRS-1 pS616 density increased with age in normal tissue but was elevated in ADd and decreased with age.
    • IRS-1 pS616 pathology positively correlated with beta-amyloid, phospho-tau, and Braak stage.
    • No significant differences in ADd pathologies were found across ApoE genotypes.

    Conclusions:

    • Brain insulin resistance, indicated by IRS-1 pS616, rises with age, peaks in ADd, and declines with neurodegeneration.
    • Cytoplasmic IRS-1 pS616 accumulation in neurons is implicated in AD pathogenesis.
    • IRS-1 pS616 may serve as a biomarker for brain insulin resistance and a target for AD therapies.