Shared proteomic effects of cerebral atherosclerosis and Alzheimer’s disease on the human brain
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Abstract
Cerebral atherosclerosis contributes to dementia via unclear processes. We performed proteomic sequencing of dorsolateral prefrontal cortex in 438 older individuals and found associations between cerebral atherosclerosis and reduced synaptic signaling and between RNA splicing and increased oligodendrocyte development and myelination. Consistently, single-cell RNA sequencing showed cerebral atherosclerosis associated with higher oligodendrocyte abundance. A subset of proteins and modules associated with cerebral atherosclerosis was also associated with Alzheimer's disease, suggesting shared mechanisms.
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Elevated levels of myelin inhibitor OMG are positively correlated with cerebral atherosclerosis and cognitive decline.
“On the other hand, elevated levels of the myelin inhibitor OMG are positively correlated with cerebral atherosclerosis and cognitive decline [78, 79].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [78]
The ‘Brain proteomic signature of cerebral atherosclerosis’ section links greater atherosclerosis to oligodendrocyte development and remyelination, but it does not identify OMG. Searches for ‘OMG,’ ‘OMgp,’ and ‘oligodendrocyte myelin glycoprotein’ found no passage in our copy relating OMG levels to either atherosclerosis or cognitive decline; no page numbers were provided. (LLM, conf=0.74)
Experimental — accuracy not yet measuredAtherosclerotic lesions in intra- and extra-cranial arteries are associated with cognitive impairment and dementia.
“In previous studies, atherosclerotic lesions in intra- and extra-cranial arteries were associated with cognitive impairment and even dementia [2,66,67].”
From Neuroprotective effect of SGLT2 inhibitors. (2021) · cites this paper as [67]
Cerebral atherosclerosis was associated with reduced synaptic function, excess myelination, and axonal injury independently of ischemia in proteomic sequencing of the dorsolateral prefrontal cortex of 438 humans.
“In reference to the proteomic sequencing of the dorsolateral prefrontal cortex of 438 humans performed by Wingo A.P. et al., CA was associated with reduced synaptic function, excess myelination, and axonal injury independently of ischemia [67].”
From Neuroprotective effect of SGLT2 inhibitors. (2021) · cites this paper as [67]
Nearly a dozen network-based analyses of the AD proteome have been performed in the human brain, including the dorsolateral prefrontal cortex, temporal cortex, and other cortical regions heavily affected in AD.
“Nearly a dozen informative network-based analyses of the AD proteome have been performed in the human brain [62–64, 74, 78, 96, 104–108], including the dorsolateral prefrontal cortex (DLPFC), temporal cortex, and other cortical regions heavily affected in AD.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
No similar statistical correlations were observed between cerebral atherosclerosis and Aβ accumulation or tau burden.
“the authors observed no similar statistical correlations between cerebral atherosclerosis and Aβ accumulation or tau burden.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
Cerebral atherosclerosis contributes to AD through oligodendrocyte dysfunction and injury to the myelin sheath, regardless of hallmark proteinopathy, gross ischemic disease, or cerebrovascular risk factors.
“Overall, these findings suggest that cerebral atherosclerosis, a common occurrence among the elderly, contributes to AD through oligodendrocyte dysfunction and injury to the myelin sheath, regardless of hallmark proteinopathy, gross ischemic disease, or cerebrovascular risk factors.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
The associations between the myelin module and cerebral atherosclerosis and AD dementia persisted after adjustment for hypertension, diabetes, and other cerebrovascular risk factors.
“These associations also persisted after adjustment for hypertension, diabetes, and other cerebrovascular risk factors.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
The oligodendrocyte-enriched myelin module was one of only two protein communities in the co-expression network associated with both cerebral atherosclerosis and AD dementia, independent of Aβ, tau tangles, infarct burden, and a variety of other pathologies.
“The oligodendrocyte-enriched myelin module was one of only two protein communities in the co-expression network associated with both cerebral atherosclerosis and AD dementia, independent of Aβ, tau tangles, infarct burden, and a variety of other pathologies.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
Wingo et al. found that cerebral atherosclerosis may be the missing link between oligodendrocytes and AD dementia.
“Wingo et al. found that cerebral atherosclerosis may be the missing link between oligodendrocytes and AD dementia [107].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [107]
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Walker, K. A., Chen, J., Shi, L., Yang, Y., Fornage, M., Zhou, L., Schlosser, P., Surapaneni, A., Grams, M. E., Duggan, M. R., et al. (2023) · Science Translational Medicine · doi:10.1126/scitranslmed.adf5681 · Cited by 148 · see citing works
Hypoxia compromises the mitochondrial metabolism of Alzheimer’s disease microglia via HIF1
March-Diaz, R., Lara-Ureña, N., Romero-Molina, C., Heras-Garvin, A., Ortega-de San Luis, C., Alvarez-Vergara, M. I., Sanchez-Garcia, M. A., Sanchez-Mejias, E., Davila, J. C., Rosales-Nieves, A. E., et al. (2021) · Nature Aging · doi:10.1038/s43587-021-00054-2 · Cited by 125 · see citing works
Cortical Proteins Associated With Cognitive Resilience in Community-Dwelling Older Persons
Yu, L., Tasaki, S., Schneider, J. A., Arfanakis, K., Duong, D. M., Wingo, A. P., Wingo, T. S., Kearns, N., Thatcher, G. R. J., Seyfried, N. T., et al. (2020) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2020.1807 · Cited by 127 · see citing works
Self-citationSystems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
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Self-citationGenetic control of the human brain proteome
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Self-citationQuantitative phosphoproteomics uncovers dysregulated kinase networks in Alzheimer’s disease
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Multi-omics analysis reveals the key factors involved in the severity of the Alzheimer’s disease
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Revisiting atherosclerosis and dementia
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- Authors
- Wingo, A. P., Fan, W., Duong, D. M., Gerasimov, E. S., Dammer, E. B., Liu, Y., Harerimana, N. V., White, B., Thambisetty, M., Troncoso, J. C., Kim, N., Schneider, J. A., Hajjar, I. M., Lah, J. J., Bennett, D. A., Seyfried, N. T., Levey, A. I., & Wingo, T. S.
- Affiliations
- Emory University (US)
- Johns Hopkins University (US)
- National Institutes of Health (US)
- Rush University Medical Center (US)
- Corresponding author
- Wingo, Aliza P.
- Seyfried, Nicholas T.
- Levey, Allan I.
- Wingo, Thomas S.
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2020-05-18
- Volume
- 23
- Issue
- 6
- Pages
- 696-700
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC7269838
- OpenAlex
- W3025717350
- Semantic Scholar
- d83024881ad172881be9e3285b078998419498a9
- Cited by
- 161
- References
- 72
- Citations by year
- 2026: 16 · 2025: 24 · 2024: 36 · 2023: 23 · 2022: 26 · 2021: 27 · 2020: 9
- FWCI
- 15.51
- Type
- journal article
- Language
- en
- Update notices
- correction (2020-06-23)
- Open access
- green
- doi.org
- Licence
- Locations
- Nature Neuroscience (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01BX003853)
- Michael J. Fox Foundation for Parkinson's Research (P30 AG10161, 11060)
- Alzheimer's Association (P50 AG025688, P30AG10161, 11060)
- Emory University (P50AG025688, AG025688)
- Weston Brain Institute (11060)
- National Institutes of Health (I01 BX003853, AG10161, AG015819, AG025688, NS055077)
- Alzheimer's Disease Research Center, Emory University (P50 AG025688, AG025688)
- National Institute on Aging (R01AG017917, P30-AG 10161, R01AG056533, AG 10161, AG046161, R01AG042210, AG057470, AG 025688, RF1AG057470, U01AG046152, R01AG057911, U19AG033655, R01AG015819, R56AG060757, P30AG010161, R21AG055844, AG057911, U01AG061357, U01AG061356, RC2AG036547, I01 BX003853, AG017917, P50AG005146, R56AG062256, U01AG046161, AG056533, AG061800, R56AG062633, P50AG025688, R01AG064233, R01AG053960, P30AG066507, R01AG061800, P30AG066511)
- National Institute of Mental Health (U01MH115484, R01MH117292)
- National Institute of Neurological Disorders and Stroke (NS055077, P30 AG10161, P30NS055077)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- cerebral atherosclerosis, Alzheimer's disease, dementia, dorsolateral prefrontal cortex, proteomics, oligodendrocytes, myelination, synaptic signaling, RNA splicing, shared pathogenesis, older adults
- MeSH terms
- Aging, Alzheimer Disease, Intracranial Arteriosclerosis, Humans, Nerve Tissue Proteins, Databases, Factual, Prefrontal Cortex, Proteomics
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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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