Beta-amyloid oligomers induce phosphorylation of tau and inactivation of insulin receptor substrate via c-Jun N-terminal kinase signaling: suppression by omega-3 fatty acids and curcumin.

@article{Ma2009BetaamyloidOI,
  title={Beta-amyloid oligomers induce phosphorylation of tau and inactivation of insulin receptor substrate via c-Jun N-terminal kinase signaling: suppression by omega-3 fatty acids and curcumin.},
  author={Qingyin Ma and Fusheng Yang and Emily R Rosario and Oliver J. Ubeda and Walter Beech and Dana J. Gant and Ping Ping Chen and Beverly Hudspeth and Cory K Chen and Yongle Zhao and H V Vinters and Sally Ann Frautschy and G. M. Cole},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2009},
  volume={29 28},
  pages={
          9078-89
        }
}
Both insulin resistance (type II diabetes) and beta-amyloid (Abeta) oligomers are implicated in Alzheimer's disease (AD). Here, we investigate the role of Abeta oligomer-induced c-Jun N-terminal kinase (JNK) activation leading to phosphorylation and degradation of the adaptor protein insulin receptor substrate-1 (IRS-1). IRS-1 couples insulin and other trophic factor receptors to downstream kinases and neuroprotective signaling. Increased phospho-IRS-1 is found in AD brain and insulin-resistant… CONTINUE READING
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