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Basic Science and Pathogenesis.

Obed Okwoli Apochi1, Rebecca Bernal2, Yannick Joel Wadop Ngouongo3

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Summary
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APOE-ε4 increases Alzheimer's disease risk, while APOE-ε2 is protective. TDP-43 proteinopathy modifies these effects, reducing APOE-ε4's impact and enhancing APOE-ε2's protection.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • The apolipoprotein E (APOE) genotype, particularly the APOE-ε4 allele, is a significant risk factor for Alzheimer's disease (AD) and influences neuropathological hallmarks.
  • However, the precise role of APOE in AD progression, considering individual variability due to factors like age and sex, requires further elucidation.

Purpose of the Study:

  • To investigate the association between APOE genotype and various neuropathological outcomes in a large cohort.
  • To explore the potential modifying effect of TDP-43 proteinopathy on the relationship between APOE genotype and AD neuropathology.

Main Methods:

  • Utilized the NACC dataset comprising 7,117 participants, categorized by APOE genotype (ε2, ε3, ε4 carriers).
  • Assessed neuropathological outcomes including Thal Phase, Braak Stage, neuritic plaques, diffuse plaques, and cerebral amyloid angiopathy using logistic regression.
  • Performed interaction analyses to evaluate the modifying role of TDP-43 proteinopathy.

Main Results:

  • APOE-ε4 carriers exhibited significantly higher odds for all examined neuropathological markers compared to ε3 homozygotes.
  • APOE-ε2 carriers demonstrated significantly reduced odds for these pathologies.
  • A significant interaction was observed between APOE and TDP-43 proteinopathy concerning neuritic plaques, where TDP-43 attenuated the effect of APOE-ε4 and enhanced the protective effect of APOE-ε2.

Conclusions:

  • TDP-43 proteinopathy modulates the genetic influence of APOE on AD neuropathology.
  • The presence of TDP-43 proteinopathy appears to reduce the risk conferred by APOE-ε4 and amplify the protective effects of APOE-ε2.
  • Further research is warranted to understand the interplay of genetic and environmental factors in AD neuropathology.