Department of Psychiatry
Immunology and Infectious Disease | Nervous System Diseases | Neurology | Neuroscience and Neurobiology | Psychiatry and Psychology | Translational Medical Research
The function of B cells in Alzheimer's disease (AD) is not fully understood. While immunoglobulins that target amyloid beta (Abeta) may interfere with plaque formation and hence progression of the disease, B cells may contribute beyond merely producing immunoglobulins. Here we show that AD is associated with accumulation of activated B cells in circulation, and with infiltration of B cells into the brain parenchyma, resulting in immunoglobulin deposits around Abeta plaques. Using three different murine transgenic models, we provide counterintuitive evidence that the AD progression requires B cells. Despite expression of the AD-fostering transgenes, the loss of B cells alone is sufficient to reduce Abeta plaque burden and disease-associated microglia. It reverses behavioral and memory deficits and restores TGFbeta(+) microglia, respectively. Moreover, therapeutic depletion of B cells at the onset of the disease retards AD progression in mice, suggesting that targeting B cells may also benefit AD patients.
B cells, Neuroimmunology, Translational immunology, Alzheimer's disease
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DOI of Published Version
Kim K, Wang X, Ragonnaud E, Bodogai M, Illouz T, DeLuca M, McDevitt RA, Gusev F, Okun E, Rogaev E, Biragyn A. Therapeutic B-cell depletion reverses progression of Alzheimer's disease. Nat Commun. 2021 Apr 12;12(1):2185. doi: 10.1038/s41467-021-22479-4. PMID: 33846335; PMCID: PMC8042032. Link to article on publisher's site
Kim K, Wang X, Ragonnaud E, Bodogai M, Illouz T, DeLuca M, McDevitt RA, Gusev F, Okun E, Rogaev EI, Biragyn A. (2021). Therapeutic B-cell depletion reverses progression of Alzheimer's disease. Open Access Publications by UMMS Authors. https://doi.org/10.1038/s41467-021-22479-4. Retrieved from https://escholarship.umassmed.edu/oapubs/4698
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This work is licensed under a Creative Commons Attribution 4.0 License.
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