Alzheimer's disease research and treatments
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It is posit that amyloid-scaffolded accumulation of numerous M42+ proteins is a central mechanism mediating downstream pathophysiology in AD, suggesting that they are pathology modifiers and thus putative therapeutic targets.
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Alzheimer's disease (AD) is a complex neurodegenerative disorder that develops over decades. AD brain proteomics reveals vast alterations in protein levels and numerous altered biologic pathways. Here, we compare AD brain proteome and network changes with the brain proteomes of amyloid β (Aβ)-depositing mice to identify conserved and divergent protein networks with the conserved networks identifying an Aβ amyloid responsome. Proteins in the most conserved network (M42) accumulate in plaques, cerebrovascular amyloid (CAA), and/or dystrophic neuronal processes, and overexpression of two M42 proteins, midkine (Mdk) and pleiotrophin (PTN), increases the accumulation of Aβ in plaques and CAA. M42 proteins bind amyloid fibrils in vitro, and MDK and PTN co-accumulate with cardiac transthyretin amyloid. M42 proteins appear intimately linked to amyloid deposition and can regulate amyloid deposition, suggesting that they are pathology modifiers and thus putative therapeutic targets. We posit that amyloid-scaffolded accumulation of numerous M42+ proteins is a central mechanism mediating downstream pathophysiology in AD.
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@article{Levites2024Integrative,
title = {Integrative proteomics identifies a conserved Aβ amyloid responsome, novel plaque proteins, and pathology modifiers in Alzheimer’s disease},
author = {Yona Levites and Eric B. Dammer and Yong Ran and Wangchen Tsering and Duc M. Duong and Measho Abreha and Joshna Gadhavi and Kiara Lolo and Jorge Trejo‐Lopez and Jennifer Phillips and Andrea Iturbe and Aya Erquizi and Brenda D. Moore and Danny Ryu and Aditya Natu and Kristy Dillon and Jose Torrellas and Corey Moran and Thomas B. Ladd and Farhana Afroz and Tariful Islam and Jaishree Jagirdar and Cory C. Funk and Max Robinson and Srikant Rangaraju and David Borchelt and Nilüfer Ertekin-Taner and Jeffery W. Kelly and Frank L. Heppner and Erik C. B. Johnson and Karen N. McFarland and Allan I. Levey and Stefan Prokop and Nicholas T. Seyfried and Todd E. Golde},
journal = {Cell Reports Medicine},
year = {2024},
doi = {10.1016/j.xcrm.2024.101669},
url = {https://doi.org/10.1016/j.xcrm.2024.101669}
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