PUBLICATIONS

Amyloid-β plaques enhance Alzheimer's brain tau-seeded pathologies by facilitating neuritic plaque tau aggregation

He Z, Guo JL, McBride JD, Narasimhan S, Kim H, Changolkar L, Zhang B, Gathagan RJ, Yue C, Dengler C, Stieber A, Nitla M, Coulter DA, Abel T, Brunden KR, Trojanowski JQ, Lee VM. Nat Med. 2017 Dec 4. doi: 10.1038/nm.4443. [Epub ahead of print]

Summary

New Alzheimer’s Animal Model More Closely Mimics Human Disease
Penn study of amyloid plaques and tau tangles aims to accelerate discovery of new therapies
By injecting human Alzheimer’s disease brain extracts of pathological tau protein (from postmortem donated tissue) into mice with different amounts of amyloid-β (Aβ) plaques in their brains, researchers from the Perelman School of Medicine at the University of Pennsylvania found that amyloid-β facilitates the interaction between the plaques and abnormal tau. This relationship promotes the spread of mutated tau proteins in neurons, which is the hallmark of long-term Alzheimer’s disease. They published their findings this week in Nature Medicine.
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