Abstract:
:Diabetes has been identified to be a risk factor for Alzheimer's disease (AD). Vildagliptin, a novel oral hypoglycemic agent, has been demonstrated to exert protective effects on the pancreas and cardiovascular system. The present study examined the potential protective effects of vildagliptin on neurons in an AD rat model. Treatment with vildagliptin improved memory deficits and decreased neuronal apoptosis in the hippocampus. The expression levels of B cell lymphoma 2 (Bcl‑2) were increased, and the expression levels of caspase‑3, Bcl‑2 associated X protein and AD‑associated proteins were decreased in the hippocampus following treatment with vildagliptin. Additionally, the AD model‑induced decrease in phosphorylated (p) protein kinase B (p‑Akt), p‑glycogen synthase kinase 3β (p‑GSK3β), post‑synaptic density 95 and synaptophysin expression was reversed. These results indicate that vildagliptin administration exerts a protective effect against cognitive deficits by reducing tau phosphorylation and increasing the expression of proteins associated with synaptic plasticity in the hippocampus. Targeting of the Akt/GSK3β signaling pathway may be a key mechanism in preventing the disease progression of AD.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Ma QH,Jiang LF,Mao JL,Xu WX,Huang Mdoi
10.3892/mmr.2017.8289subject
Has Abstractpub_date
2018-03-01 00:00:00pages
4113-4119issue
3eissn
1791-2997issn
1791-3004journal_volume
17pub_type
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