الفهرس 
Study of The Possible Neuroprotective Effects of Vildagliptin on Drug Induced Alzheimer’s Disease in Rats with Metabolic Syndrome: Role of Hippocampal Klotho Protein Regulation
ContentsOnly 14 pages are availabe for public view
 |  | from | 238 |  |  |
| | | from | 238 | | |
Abstract
Many growing evidences suggest the presence of several similarities in the molecular mechanisms underlying the neurodegenerative diseases and metabolic abnormalities. Adults who develop Metabolic Syndrome (MS) at later stages are at a higher risk of developing Alzheimer{u2019}s disease (AD). Pharmacological agents, like dipeptidyl peptidase-4 (DPP-4) inhibitors that increase the levels of glucagon like peptide 1 (GLP-1) and ameliorate symptoms of MS, have become an auspicious candidate as disease modifying agents in the treatment of AD. The present study investigates the beneficial effects of Vildagliptin (VIG), a DPP-4 inhibitor in counteracting cognitive decline in different models of dementia targeting the protein kinase B (AKT), janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathways and hippocampal Klotho expression, to judge the potential neuroprotective, anti-apoptotic and anti-inflammatory effects of the drug. Cognitive decline was induced by administration of high fat high fructose (HFHF) diet along the experiment alone and oral administration of aluminium chloride (AlCl3) (100 mg/kg/day) for 60 days (combined or separated). Rats were orally administered VIG (10mg/kg) for 60 days along with AlCl3 administration. VIG treatment markedly improved spatial memoryand activities compared to control groups in Morris water maze (MWM) test and open field test respectively. Results revealed an increase of both hippocampal klotho and B-cell lymphoma 2 (Bcl-2) expressions along with an increase in both AKT and extracellular signal-regulated kinase (ERK) phosphorylation in VIG-treated compared to control groups