# The association of human apolipoprotein ε4 with dementia, cognition, imaging, and plasma biomarkers of neurodegeneration in a sample of older adults in the Democratic Republic of the Congo

**Authors:** Jean Ikanga, Saranya Sundaram Patel, Megan Schwinne, Caterina Alessandra Obenauf, Emmanuel Epenge, Guy Gikelekele, Nathan Tshengele, Immaculee Kavugho, Samuel Mampunza, Lelo Mananga, Charlotte E. Teunissen, Julio C. Rojas, Brandon Chan, Argentina Lario Lago, Adam L. Boxer, Andreas Jeromin, Emile Omba, Alden L. Gross, Alvaro Alonso

PMC · DOI: 10.1002/alz.70735 · 2025-10-14

## TL;DR

This study found that the APOE ε4 allele is linked to dementia and cognitive decline in older adults from the Democratic Republic of the Congo.

## Contribution

The study is one of the first to investigate APOE ε4's role in neurodegeneration in an African population.

## Key findings

- APOE ε4 carriers showed greater cognitive decline and hippocampal atrophy.
- Dementia cases had higher APOE ε4 prevalence and elevated plasma biomarker levels.
- Findings highlight APOE ε4's significant impact on neurodegeneration in African populations.

## Abstract

This study examined the association between the apolipoprotein E (APOE) ε4 allele and cognitive performance, neuroimaging, and plasma biomarkers in Congolese older adults in the Democratic Republic of the Congo (DRC).

Eighty‐four participants (39 healthy controls [HCs], 45 with suspected dementia), aged 73.0 years on average, were assessed using the African Neuropsychology Battery, magnetic resonance imaging, and blood‐based biomarkers. Regression models adjusted for age, sex, and education evaluated APOE’s impact.

APOE ε4 was more prevalent in dementia cases than in HCs. Overall, APOE ε4 status significantly affected naming and memory scores, mesial temporal and entorhinal cortex atrophy scores, and glial fibrillary acidic protein concentration levels. In HCs, it showed no significant impact on cognitive or neuroimaging tests, except for neurofilament light chain concentration levels. Among dementia participants, APOE ε4 status influenced only naming and memory scores.

APOE ε4 carriers in this DRC cohort showed greater cognitive decline and neurodegeneration, highlighting its significant impact in African populations.

Apolipoprotein E (APOE) ε4 was more frequent in dementia cases than in healthy controls in a Democratic Republic of the Congo cohort.
APOE ε4 carriers showed greater cognitive decline, especially in memory and visuospatial skills.Neuroimaging findings revealed increased hippocampal atrophy and cortical thinning in carriers.Plasma biomarkers in dementia showed higher amyloid beta 40, phosphorylated tau181, neurofilament light chain, and tumor necrosis factor alpha levels.Findings underscore APOE ε4's impact on neurodegeneration in African populations.

Apolipoprotein E (APOE) ε4 was more frequent in dementia cases than in healthy controls in a Democratic Republic of the Congo cohort.

APOE ε4 carriers showed greater cognitive decline, especially in memory and visuospatial skills.

Neuroimaging findings revealed increased hippocampal atrophy and cortical thinning in carriers.

Plasma biomarkers in dementia showed higher amyloid beta 40, phosphorylated tau181, neurofilament light chain, and tumor necrosis factor alpha levels.

Findings underscore APOE ε4's impact on neurodegeneration in African populations.

## Linked entities

- **Genes:** APOE (apolipoprotein E) [NCBI Gene 348]
- **Diseases:** dementia (MONDO:0001627)

## Full-text entities

- **Genes:** APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}
- **Diseases:** atrophy (MESH:D001284), dementia (MESH:D003704), neurodegeneration (MESH:D019636), cognitive decline (MESH:D003072)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12519526/full.md

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Source: https://tomesphere.com/paper/PMC12519526