Clonal hematopoiesis, aging and Alzheimer’s disease
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CHIP-associated mutations in genes such as DNMT3A, TET2, and ASXL1 promote chronic inflammation, endothelial dysfunction, and accelerated atherogenesis through altered myeloid cell function and cytokine signaling.
“CHIP-associated mutations in genes such as DNMT3A, TET2, and ASXL1 promote chronic inflammation, endothelial dysfunction, and accelerated atherogenesis through altered myeloid cell function and cytokine signaling [7,15,43]”
Competing risks play a decisive role: CHIP carriers experience increased cardiovascular morbidity and mortality, effectively limiting survival to ages at which clinical AD is most frequently diagnosed.
“First, competing risks play a decisive role: CHIP carriers experience increased cardiovascular morbidity and mortality, effectively limiting survival to ages at which clinical AD is most frequently diagnosed [4,7].”
CHIP-associated cardiovascular mortality may prevent carriers from reaching the advanced ages at which AD is typically diagnosed.
“As previously discussed, CHIP-associated cardiovascular mortality may prevent carriers from reaching the advanced ages at which AD is typically diagnosed [7,15].”
Other CHIP mutations, or identical mutations operating in different biological contexts, may exacerbate systemic inflammation, endothelial dysfunction, and cardiovascular pathology, indirectly increasing susceptibility to neurodegeneration through vascular injury and reduced cerebrovascular reserve.
“Conversely, other CHIP mutations, or identical mutations operating in different biological contexts, may exacerbate systemic inflammation, endothelial dysfunction, and cardiovascular pathology, indirectly increasing susceptibility to neurodegeneration through vascular injury and reduced cerebrovascular reserve [7,15].”
Recent geroscience syntheses have identified clonal hematopoiesis as a systemic driver of inflammaging and vascular aging, with pleiotropic effects observed across organ systems, including the brain.
“Recent geroscience syntheses have identified clonal hematopoiesis as a systemic driver of inflammaging and vascular aging, with pleiotropic effects observed across organ systems, including the brain [7].”
Cites
Clonal hematopoiesis in human aging and disease
Jaiswal, S., & Ebert, B. L. (2019) · Science · doi:10.1126/science.aan4673 · Cited by 1,156 · see citing works
Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6
Zhang, Q., Zhao, K., Shen, Q., Han, Y., Gu, Y., Li, X., Zhao, D., Liu, Y., Wang, C., Zhang, X., et al. (2015) · Nature · doi:10.1038/nature15252 · Cited by 807 · see citing works
Self-citationClonal hematopoiesis is associated with protection from Alzheimer’s disease
Bouzid, H., Belk, J. A., Jan, M., Qi, Y., Sarnowski, C., Wirth, S., Ma, L., Chrostek, M. R., Ahmad, H., Nachun, D., et al. (2023) · Nature Medicine · doi:10.1038/s41591-023-02397-2 · Cited by 169 · see citing works
TET2 Regulates the Neuroinflammatory Response in Microglia
Carrillo-Jimenez, A., Deniz, Ö., Niklison-Chirou, M. V., Ruiz, R., Bezerra-Salomão, K., Stratoulias, V., Amouroux, R., Yip, P. K., Vilalta, A., Cheray, M., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.09.013 · Cited by 104 · see citing works
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Kopp, K., Silva, P., Damm, F., & Cosma, N. C. (2026) · Biomedicines · doi:10.3390/biomedicines14051012
- Authors
- Sánchez Vela, P., Trowbridge, J. J., & Levine, R. L.
- Affiliations
- Jackson Laboratory (US)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Levine, Ross L.
- Venue
- Nature Medicine
- Published
- 2023-07
- Volume
- 29
- Issue
- 7
- Pages
- 1605-1606
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W4383066730
- Cited by
- 8
- References
- 4
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3
- FWCI
- 1.65
- Type
- journal article
- Language
- en
- Update notices
- correction (2023-11-20)
- Open access
- closed
- Licence
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- National Institute on Aging (R01AG069010, U01AG077925)
- National Cancer Institute (P30CA008748, P30CA034196)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK118072)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- clonal hematopoiesis, Alzheimer's disease, aging, age-related diseases, disease protection, hematopoietic stem cells
- MeSH terms
- Clonal Hematopoiesis, Aging, Alzheimer Disease, Cardiovascular Diseases, Hematopoiesis, Humans, Mutation
About these checks
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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