AI Article Synopsis
- The connection between diabetes mellitus (DM) and Alzheimer's disease (AD) involves the role of amyloid deposits and the enzyme glycogen synthase kinase-3 (GSK-3).
- Research on DM rats shows increased GSK-3 activity and decreased Akt activity, leading to overproduction of amyloid-β peptides and hyperphosphorylation of tau protein in the hippocampus.
- Inhibiting GSK-3 with lithium can reduce these processes, indicating that GSK-3 may be a factor in the neurological complications seen in DM that resemble AD.
Article Abstract
The pathogenesis of diabetic neurological complications is not fully understood. Diabetes mellitus (DM) and Alzheimer's disease (AD) are characterized by amyloid deposits. Glycogen synthase kinase-3 (GSK-3) plays an important role in the pathogenesis of AD and DM. Here we tried to investigate the production of amyloid-β peptides (A β) and phosphorylation of microtubule-associated protein tau in DM rats and elucidate the role of GSK-3 and Akt (protein kinase B, PKB) in these processes. Streptozotocin injection-induced DM rats displayed an increased GSK-3 activity, decreased activity and expression of Akt. And A β 40 and A β 42 were found overproduced and the microtubule-associated protein tau was hyperphosphorylated in the hippocampus. Furthermore, selective inhibition of GSK-3 by lithium could attenuate the conditions of A β overproduction and tau hyperphosphorylation. Taken together, our studies suggest that GSK-3 regulates both the production of A β and the phosphorylation of tau in rat brain and may therefore contribute to DM caused AD-like neurological defects.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3997149 | PMC |
| http://dx.doi.org/10.1155/2014/878123 | DOI Listing |
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