Extended Data Fig. 10: B2M is an essential factor for Aβ neurotoxicity and a novel target for therapeutic intervention in AD. | Nature Neuroscience

Extended Data Fig. 10: B2M is an essential factor for Aβ neurotoxicity and a novel target for therapeutic intervention in AD.

From: β2-Microglobulin coaggregates with Aβ and contributes to amyloid pathology and cognitive deficits in Alzheimer’s disease model mice

Extended Data Fig. 10: B2M is an essential factor for Aβ neurotoxicity and a novel target for therapeutic intervention in AD.The alternative text for this image may have been generated using AI.

Elevation of B2M aggravates amyloid pathology independent of MHC-I, and coaggregation with B2M is essential for Aβ neurotoxicity. Importantly, both peripheral and brain B2M contribute to AD pathogenesis. Therapeutically, ASO or monoclonal antibody-mediated B2M depletion mitigates AD-associated neuropathology, and inhibiting B2M-Aβ coaggregation with a B2M-based blocking peptide ameliorates amyloid pathology and cognitive deficits in AD mice.

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