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Basic Science and Pathogenesis.

Rebecca Bernal1, Obed Okwoli Apochi2, Yannick Joel Wadop Ngouongo3,4

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Summary
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The Apolipoprotein E (APOE) ε4 allele is linked to increased arteriolosclerosis and hippocampal sclerosis risk. APOE ε2 carriers face higher odds of large arterial infarcts. TDP-43 proteinopathy influences these associations.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
  • Apolipoprotein E (APOE) genotype is implicated in AD pathogenesis.
  • Limited research exists on APOE's role in cerebral vascular pathology.

Purpose of the Study:

  • Investigate the association between APOE genotypes and specific vascular pathology lesions.
  • Examine the influence of TDP-43 proteinopathy on APOE-vascular pathology relationships.
  • Utilize the National Alzheimer's Coordinating Center (NACC) dataset for comprehensive analysis.

Main Methods:

  • Analysis of NACC data from 7117 participants.
  • Classification of participants by APOE genotype (ε4 carriers, ε3 homozygotes, ε2 carriers).
  • Logistic regression models adjusted for demographic factors, assessing arteriolosclerosis, atherosclerosis, large arterial infarcts, lacunes, hippocampal sclerosis, and microbleeds.
  • Evaluation of effect modification by TDP-43 proteinopathy status.

Main Results:

  • APOE ε4 carriers showed increased odds of arteriolosclerosis (OR 1.19) and hippocampal sclerosis (OR 1.28) compared to ε3 homozygotes.
  • APOE ε2 carriers had increased odds of large arterial infarcts (OR 1.71).
  • TDP-43 proteinopathy significantly modified the association between APOE genotype and arteriolosclerosis/hippocampal sclerosis. APOE ε4 carriers with absent TDP-43 had higher arteriolosclerosis odds (OR 1.37).

Conclusions:

  • APOE ε4 allele increases arteriolosclerosis and hippocampal sclerosis risk.
  • APOE ε2 allele is associated with a higher risk of large arterial infarcts.
  • TDP-43 proteinopathy modulates these APOE-related vascular and neurodegenerative effects, particularly in individuals without TDP-43 pathology.