Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (6): 2343-2344.doi: 10.4103/NRR.NRR-D-25-00503

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BAG3 in traumatic brain injury: a cell-type-specific modulator of tau hyperphosphorylation#br#

Nicholas Sweeney, Tae Yeon Kim, Hongjun Fu*   

  1. Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, OH, USA (Sweeney N, Kim TY, Fu H)
    Biomedical Sciences Graduate Program, College of Medicine, The Ohio State University, Columbus, OH, USA (Kim TY)
    Chronic Brain Injury Institute, The Ohio State University, Columbus, OH, USA (Fu H)
  • Online:2026-06-15 Published:2026-04-16
  • Contact: Hongjun Fu, PhD, Hongjun.Fu@osumc.edu.
  • Supported by:
    This work was supported by the award W81XWH1910309 (to HF) from the Department of Defense, the award R01-AG075092-01 (to HF) and the award RF1AG063521 from the National Institute of Aging at the National Institutes of Health, the Neurological Research Institute Seed grant (to HF) from The Ohio State University, and the Summer Undergraduate Research Fellowship (to NS) from The Ohio State University Chronic Brain Injury Discovery Theme.

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Abstract: BCL2-associated anthanogene 3 facilitates the clearance of tau protein aggregates: BCL2-associated anthanogene 3 (BAG3) is a ubiquitously expressed and highly conserved multi-functional co-chaperone protein involved in many biological processes that supports cellular homeostasis, including the inhibition of apoptosis by preventing mitochondrial BAX localization (Lin et al., 2022) and the promotion of the degradation of hyperphosphorylated tau aggregates by its interactions with SQSTM1 (p62) (Hamano and Mutoh, 2022).