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• W2896668068 abstract "Increasing evidence supports the implication of insulin signaling alterations in the development of Alzheimeŕs disease (AD). Insulin is related with tau protein phosphorylation and Aβ clearance, thus participating in the regulation of two major hallmarks of AD. Our group has previously demonstrated that Thioredoxin-80 (Trx80), which is dramatically decreased in AD brains, has an anti-amyloidogenic effect on Aβ and prevents its toxicity. We have recently reported a new pathological mechanism in AD that involves insulin accumulation as oligomers in NFT-bearing neurons, leading to insulin resistance. We hypothesize that Trx80 could also prevent insulin aggregation, and thus play a key role in the development of insulin signaling and glucose metabolism alterations reported in AD. Primary cultures, western blot, MTT assay, immunofluorescence, electron microscopy, Thioflavin T assay, qPCR. We show that Trx80 prevents insulin aggregation in vitro, and rescues the loss of function of aggregated insulin. Insulin and Trx80 co-localize in human pancreas and neurons, what suggests the interaction of both proteins in vivo. Furthermore, Trx80 overexpression prevents okadaic acid-mediated insulin accumulation in SH-SY5Y neuroblastoma cells. These results suggest a key role for Trx80 in the regulation of insulin signaling and glucose metabolism, although the molecular mechanisms and its role in pathological conditions remains to be fully investigated." @default.
• W2896668068 created "2018-10-26" @default.
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• W2896668068 date "2018-07-01" @default.
• W2896668068 modified "2023-10-16" @default.
• W2896668068 title "P2‐155: THIOREDOXIN 80 MAINTAINS INSULIN ACTIVITY BY PREVENTING ITS AGGREGATION: IMPLICATIONS FOR ALZHEIMER'S DISEASE" @default.
• W2896668068 doi "https://doi.org/10.1016/j.jalz.2018.06.842" @default.
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