Novel Neuro protective mechanism of Flupirtine against 3-NPA induced memory impairment and motor incoordination in experimental model of Huntington’s disease.

Abstract

Huntington’s Disease (HD) is a progressive neurodegenerative disorder that gradually declines cognitive skills, impair memory and normal movements of affected individuals. Huntington’s Disease (HD) is an autosomal dominant inherited disease caused by the repetition of CAG repeats on the short arm of chromosome 4p16.3 in huntingtin gene (Htt). On the Morris Water Maze test, 3-NPA treated group rats finds the platform in less time than control & Flupirtine group i.e. their spatial & learning memory was more than control group rats. The significant difference was found at Probe trial day between 3-NPA and Flupirtine group. Flupirtine treated rats at high dose spent more time in open arm than 3-NPA treated rats and less time in dark arm then 3-NPA treated rats. 3-NPA showed decreased retention time on the rotating rod than the control group & Flupirtine at high dose treated rats showed increased retention time on the rotating rod. Decreased GSH levels were observed in 3-NPA treated group than control group rats and Flupirtine at high dose increased the level of GSH in 3- NPA treated rats. High level of MDA was found in 3-NPA rats than control group rats and found to be low in the Flupirtine treated group. Flupirtine increase the level of SOD in 3- NPA treated rats as it was reduced due to the toxicity of 3- NPA. Low levels of CAT were also observed in 3- NPA treated rats compared to control group and Flupirtine increases the level of CAT in 3- NPA treated rats. Keywords: Huntington’s Disease, Flupirtine, Morris Water Maze test, huntingtin gene, 3- Nitropropanoic acid (3-NPA), neurodegenerative disorder.