Plasma apolipoprotein E levels, isoform composition, and dimer profile in relation to plasma lipids in racially diverse patients with Alzheimer’s disease and mild cognitive impairment
Open accessAbstract
Background: The APOE ε4-promoted risk of Alzheimer’s disease (AD) is lower in Black/African-Americans (B/AAs), compared to non-Hispanic whites (NHWs). Previous studies reported lower plasma apolipoprotein E (apoE) levels in NHW APOE ε4-carriers compared to non-carriers, and low plasma apoE levels were directly associated with an increased risk of AD and all dementia. We further showed that APOE ε3/ε3 AD patients exhibited reduced plasma apoE dimers compared to corresponding control subjects. Whether plasma apoE levels and apoE dimer formation differ between races/ethnicities and therefore may help explain AD risk racial disparity remains to be elucidated. Methods: Using mass spectrometry, we determined total plasma apoE and apoE isoform levels in a cohort of B/AAs (n = 58) and NHWs (n = 67) including subjects with normal cognition (B/AA: n = 25, NHW: n = 28), mild cognitive impairment (MCI) (B/AA: n = 24, NHW: n = 24), or AD dementia (B/AA: n = 9, NHW: n = 15). Additionally, we used non-reducing western blot analysis to assess the distribution of plasma apoE into monomers/disulfide-linked dimers. Plasma total apoE, apoE isoform levels, and % apoE monomers/dimers were assessed for correlations with cognition, cerebrospinal fluid (CSF) AD biomarkers, sTREM2, neurofilament light protein (NfL), and plasma lipids. Results: Plasma apoE was predominantly monomeric in both racial groups and the monomer/dimer distribution was not affected by disease status, or correlated with CSF AD biomarkers, but associated with plasma lipids. Plasma total apoE levels were not related to disease status and only in the NHW subjects we observed lower plasma apoE levels in the APOEε 4/ε4-carriers. Total plasma apoE levels were 2.6-fold higher in B/AA compared to NHW APOE ε4/ε4 subjects and associated with plasma high-density lipoprotein (HDL) in NHW subjects but with low-density lipoprotein levels (LDL) in the B/AA subjects. Higher plasma apoE4 levels, exclusively in APOE ε3/ε4 B/AA subjects, were linked to higher plasma total cholesterol and LDL levels. In the controls, NHWs and B/AAs exhibited opposite associations between plasma apoE and CSF t-tau. Conclusions: The previously reported lower APOE ε4-promoted risk of AD in B/AA subjects may be associated with differences in plasma apoE levels and lipoprotein association. Whether differences in plasma apoE levels between races/ethnicities result from altered APOE ε4 expression or turnover, needs further elucidation.
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These findings closely mirror observations from human studies, underscoring the validity and translatability of these rat models.
“While further investigation into these mechanisms is warranted, these findings closely mirror observations from human studies, underscoring the validity and translatability of these rat models [58, 70, 71].”
From Analysis of early effects of human APOE isoforms on Alzheimer’s disease and type III hyperlipoproteinemia pathways using knock-in rat models with humanized APP and APOE (2024) · cites this paper as [71]
The Results (Table 4; page not available in our copy) report human observations linking plasma apoE with plasma lipids. The paper does not compare those observations with findings from the cited rat models or establish the models’ validity or translatability. (LLM, conf=0.78)
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Wang, R., Zhan, Y., Zhu, W., Yang, Q., & Pei, J. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1407980 · Cited by 24 · see citing works
Lin, C., Kong, Y., Chen, Q., Zeng, J., Pan, X., & Miao, J. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1420731 · Cited by 25 · see citing works
APOE genotype dictates lipidomic signatures in primary human hepatocytes
Almeida, F., Patra, K., Giannisis, A., Niesnerova, A., Nandakumar, R., Ellis, E. C. S., Oliveira, T. G., & Nielsen, H. M. (2024) · Journal of Lipid Research · doi:10.1016/j.jlr.2024.100498 · Cited by 14 · see citing works
Self-citationYesiltepe, M., Yin, T., Tambini, M., Bao, H., Pan, M., d’Abramo, C., Giliberto, L., Han, X., & D’Adamio, L. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01832-2 · Cited by 10 · see citing works
“While further investigation into these mechanisms is warranted, these findings closely mirror observations from human studies, underscoring the validity and trans-latability of these rat models [58, 70, 71].”
ResultZhao, B., Zang, P., Quan, M., Wang, Q., Guo, D., Jia, J., & Wang, W. (2025) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.70202 · Cited by 4 · see citing works
Lou, Y., Chen, X., Zhao, L., Xuc, N., Zhang, L., Hu, W., & Qiu, Y. (2024) · Frontiers in Nutrition · doi:10.3389/fnut.2024.1378959 · Cited by 3 · see citing works
Self-citationGiannisis, A., Al-Grety, A., Carlsson, H., Howell, J. C., Hu, W. T., Kultima, K., & Nielsen, H. M. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01306-6 · Cited by 1 · see citing works
Self-citationLa colección de libros cabalísticos de la editorial Maucci
Vicente, F. F. C. (2009) · Hibris: Revista de bibliofilia
Raber, J., & Nielsen, H. M. (2025) · Springer eBooks · doi:10.1007/978-3-031-52641-1_41-1
Self-citationRaber, J., & Nielsen, H. M. (2026) · Springer eBooks · doi:10.1007/978-3-031-96089-5_41
Self-citationBurman, J., Fan, C., Husseiny, M. E., Riestra, P. V., Sandberg, A., Zambirinis, C. P., Kotán, R., Amorim, L., Gimm, O., & Bojmar, L. (2026) · iScience · doi:10.1016/j.isci.2026.116723
- Authors
- Giannisis, A., Al-Grety, A., Carlsson, H., Howell, J. C., Hu, W. T., Kultima, K., & Nielsen, H. M.
- Affiliations
- Stockholm University (SE)
- Uppsala University (SE)
- Emory University (US)
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Nielsen, Henrietta M.
- ORCID
- Venue
- Alzheimer's Research & Therapy
- Published
- 2023-07-03
- Volume
- 15
- Issue
- 1
- Pages
- 119-119
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC10316569
- OpenAlex
- W4382987220
- Cited by
- 11
- References
- 77
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 1
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Update notices
- correction (2023-09-27)
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- KTH Publication Database DiVA (KTH Royal Institute of Technology) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- BrightFocus Foundation (A2019446S)
- Olle Engkvists Stiftelse
- Demensfonden
- Stockholm University
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- apolipoprotein E, APOE isoforms, Alzheimer's disease, mild cognitive impairment, racial disparities, Black patients, plasma lipids, HDL cholesterol, LDL cholesterol, APOE genotype, sTREM2, neurofilament light chain, cerebrospinal fluid biomarkers
- MeSH terms
- White, Alzheimer Disease, Apolipoproteins E, Black or African American, Humans, Biomarkers, Amyloid beta-Peptides, tau Proteins, Neurofilament Proteins, Protein Isoforms, Apolipoprotein E4, Cognitive Dysfunction
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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