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Insulin resistance in the brain is linked to Alzheimer's disease (AD). This study found that the more efficient IR-B isoform of the insulin receptor is predominant in the entorhinal cortex of AD brains, possibly as a compensatory mechanism.

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • Insulin resistance and impaired insulin signaling are linked to Alzheimer's disease (AD) pathogenesis.
  • Brain insulin receptor (IR) activation enhances neural resilience, cognition, and learning.
  • IR splice variants (IR-A and IR-B) may influence insulin resistance.

Purpose of the Study:

  • To investigate the distribution and specificity of IR beta subunit antibodies in human brain tissue.
  • To quantify the expression of IR-A and IR-B isoforms in neurons of the entorhinal cortex (EC) and middle temporal gyrus (MTG) in normal aging and AD.
  • To explore the role of IR isoforms in brain insulin resistance and AD.

Main Methods:

  • Immunohistochemistry using IR beta subunit antibodies on post-mortem human brain tissue.
  • RNAscope in situ hybridization to identify and quantify IR-A and IR-B mRNA in neurons.
  • Analysis of tissue from aged normal and AD individuals in the EC and MTG.

Main Results:

  • IR beta subunit immunoreactivity was observed in neurons and astrocytes, but not other glial cells.
  • Both IR-A and IR-B mRNA isoforms were abundant in neurons in both normal and AD brains.
  • The IR-B (Exon 11+) isoform was predominant in the EC of AD brains compared to controls.

Conclusions:

  • The study identified neuronal expression of IR isoforms and characterized IR antibody binding in the human brain.
  • Predominance of the IR-B isoform in the AD entorhinal cortex suggests a potential compensatory response to brain insulin resistance.
  • These findings contribute to understanding the molecular mechanisms underlying brain insulin resistance in Alzheimer's disease.