Young bone marrow transplantation preserves learning and memory in old mice
Open accessAbstract
Restoration of cognitive function in old mice by transfer of blood or plasma from young mice has been attributed to reduced C–C motif chemokine ligand 11 (CCL11) and β2-microglobulin, which are thought to suppress neurogenesis in the aging brain. However, the specific role of the hematopoietic system in this rejuvenation has not been defined and the importance of neurogenesis in old mice is unclear. Here we report that transplantation of young bone marrow to rejuvenate the hematopoietic system preserved cognitive function in old recipient mice, despite irradiation-induced suppression of neurogenesis, and without reducing β2-microglobulin. Instead, young bone marrow transplantation preserved synaptic connections and reduced microglial activation in the hippocampus. Circulating CCL11 levels were lower in young bone marrow recipients, and CCL11 administration in young mice had the opposite effect, reducing synapses and increasing microglial activation. In conclusion, young blood or bone marrow may represent a future therapeutic strategy for neurodegenerative disease.
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Transplantation of young bone marrow preserves synaptic connections and cognitive manifestations in aged mice, increasing maximum lifespan by 30%.
“transplantation of young bone marrow plays a positive role in preserving synaptic connections and cognitive manifestations in aged mice,454 increasing the maximum lifespan by 30%.455”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [454]
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- Authors
- Das, M. M., Godoy, M., Chen, S., Moser, V. A., Avalos, P., Roxas, K. M., Dang, I., Yáñez, A., Zhang, W., Bresee, C., Arditi, M., Liu, G. Y., Svendsen, C. N., & Goodridge, H. S.
- Affiliations
- Cedars-Sinai Medical Center (US)
- Corresponding author
- Svendsen, Clive N.
- Goodridge, Helen S.
- ORCID
- Venue
- Communications Biology
- Published
- 2019-02-20
- Volume
- 2
- Issue
- 1
- Pages
- 73-73
- ISSN
- 2399-3642 (ISSN-L)
- PMC
- PMC6382867
- OpenAlex
- W2916213038
- Cited by
- 98
- References
- 42
- Citations by year
- 2026: 12 · 2025: 19 · 2024: 12 · 2023: 14 · 2022: 10 · 2021: 12 · 2020: 17 · 2019: 2
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Communications Biology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Cedars-Sinai Medical Center
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- bone marrow transplantation, cognitive aging, learning and memory, eotaxin, beta2-microglobulin, neurogenesis, synaptic connectivity, microglial activation, hippocampus, irradiation, neurodegenerative diseases, young blood
- MeSH terms
- Age Factors, Aging, Animals, beta 2-Microglobulin, Cognition, Hippocampus, Learning, Male, Memory, Mice, Inbred C57BL, Mice, Transgenic, Rejuvenation, Bone Marrow Transplantation, Mice, Congenic, Chemokine CCL11, Neurogenesis
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