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Basic Science and Pathogenesis.

Katrina Celis1, Maria Muniz2, Farid Rajabli3

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Summary
This summary is machine-generated.

Mitochondrial processes differ between European and African ancestry individuals with Alzheimer disease (AD) carrying the APOEε4 gene. These ancestry-based mitochondrial differences may explain varying AD risk between populations.

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Area of Science:

  • Neuroscience
  • Genetics
  • Mitochondrial Biology

Background:

  • APOEε4 is the strongest genetic risk factor for Alzheimer disease (AD), but its associated risk varies across ancestries.
  • African ancestry (AF) individuals exhibit lower AD risk compared to European ancestry (EU) individuals, suggesting ancestry-specific biological mechanisms.
  • Mitochondrial dysfunction is implicated in AD pathogenesis, yet its role in ancestry-biased risk remains unclear.

Purpose of the Study:

  • To investigate whether mitochondrial processes (MtFx) associated with AD are influenced by ancestry in AD patients carrying the APOEε4 allele.
  • To explore the role of mitochondria in the differential risk of AD observed between individuals of African and European ancestry.

Main Methods:

  • Single nuclei RNA sequencing (snRNA-seq) was performed on frontal cortex samples from AD patients with homozygous APOEε4 and either European Local Ancestry (EU-LA) or African Local Ancestry (AF-LA).
  • Differential gene expression analysis was conducted to compare AF-LA and EU-LA samples.
  • MitoXplorer and REACTOME tools were utilized to identify differential mitochondrial processes and construct regulatory networks.

Main Results:

  • Cells with high APOE expression (astrocytes, microglia, vascular leptomeningeal cells) showed increased expression of nuclear and mitochondrial-encoded mitochondrial (MT) genes in EU-LA compared to AF-LA samples.
  • A significant increase in pro-apoptotic, oxidative phosphorylation, and mitophagy MT-genes was observed in EU-LA samples.
  • The transcriptional regulator PPARG was identified as a potential mediator of APOEε4 effects in these cells.

Conclusions:

  • Ancestry-specific analysis of snRNA-seq in AD provides insights into mitochondrial process alterations in APOEε4 carriers.
  • Differences in mitochondrial processes influenced by ancestry may underlie the observed disparities in AD risk between European and African populations.
  • Further research is needed to determine if these transcriptional differences in mitochondrial gene expression correlate with higher APOE expression levels in European individuals.