![]() Although resident microglial cells phagocytize extracellular Aβ plaques with the help of astrocytes and TGFβ (refs. It is associated with impaired clearance of toxic protein aggregates from the brain parenchyma, such as amyloid-β (Aβ) peptides of aberrantly cleaved amyloid precursor protein (APP) 1. 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.Īlzheimer’s disease (AD) is a progressive neurodegenerative disease that mostly affects elderly people. It reverses behavioral and memory deficits and restores TGFβ + microglia, respectively. Despite expression of the AD-fostering transgenes, the loss of B cells alone is sufficient to reduce Aβ plaque burden and disease-associated microglia. Using three different murine transgenic models, we provide counterintuitive evidence that the AD progression requires B cells. 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. 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. The function of B cells in Alzheimer’s disease (AD) is not fully understood.
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