Therapeutic B-cell depletion reverses progression of Alzheimer’s disease

Ki Kim, Xin Wang, Emeline Ragonnaud, Monica Bodogai, Tomer Illouz, Marisa DeLuca, Ross A. McDevitt, Fedor Gusev, Eitan Okun, Evgeny Rogaev and Arya Biragyn ()
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Ki Kim: National Institute on Aging
Xin Wang: National Institute on Aging
Emeline Ragonnaud: National Institute on Aging
Monica Bodogai: National Institute on Aging
Tomer Illouz: The Mina and Everard Goodman faculty of Life Sciences
Marisa DeLuca: National Institute on Aging
Ross A. McDevitt: National Institute on Aging
Fedor Gusev: Institute of General Genetics, Russian Academy of Sciences
Eitan Okun: The Mina and Everard Goodman faculty of Life Sciences
Evgeny Rogaev: Institute of General Genetics, Russian Academy of Sciences
Arya Biragyn: National Institute on Aging

Nature Communications, 2021, vol. 12, issue 1, 1-11

Abstract: Abstract The function of B cells in Alzheimer’s disease (AD) is not fully understood. While immunoglobulins that target amyloid beta (Aβ) 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 Aβ 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 Aβ plaque burden and disease-associated microglia. It reverses behavioral and memory deficits and restores TGFβ+ 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.

Date: 2021
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DOI: 10.1038/s41467-021-22479-4

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