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P4‐158: Resveratrol attenuates insulin resistance‐induced cognitive deficits in rats
Author(s) -
Kamal Anand,
Chopra Kanwaljit
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.1865
Subject(s) - insulin resistance , medicine , endocrinology , resveratrol , insulin , morris water navigation task , neuroprotection , insulin receptor , oxidative stress , pharmacology , hippocampus
Background:Alzheimer’s disease (AD), the most common form of dementia, is characterized by the loss of normal functions of brain cells and neuronal death, ultimately leading to memory loss. Recent accumulating evidences have demonstrated the therapeutic potential of anti-diabetic agents, such as dipeptidyl peptidase-4 (DPP-4) inhibitors, for the treatment of Alzheimer’s disease (AD), providing opportunities to explore and test the DPP-4 inhibitors for treating this fatal disease. Prior studies determining the efficacy of Pterocarpus marsupium (PM, Fabaceae) extract for ameliorating type 2diabetes have demonstrated the DPP-4 inhibitory properties indicating the possibility of using of the extract even for the treating AD. Therefore, in the present study, the neuroprotective roles of PM for ameliorating the streptozotocin (STZ) induced AD have been tested in rat model. Methods:Experimentally, PM extract, at a dose range of 200 and 400 mg/kg, were administered orally to STZ induced AD Wistar rats and cognitive evaluation tests were performed using radial arm maze and hole-board apparatus. Pathological features including amyload load, total tau and neuroinflammation were estimated in the hippocampus. Results: Reversal of cognitive impairment was observed during treatment with PM. Following 30 days of treatment with the extracts, a doseand time-dependent attenuation of AD pathology, as evidenced by decreasing amyloid beta 42, total tau, phosphorylated tau and neuro-inflammation with an increase in glucagon-like peptide-1 (GLP-1) levels was observed. Histology of hippocampus also supports the behavioral and biochemical assesments following 30 days treatment with PM extract. Conclusions: Altogether, PM extract contain cognitive enhancers as well as neuroprotective agents against STZ induced AD.