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Abstract

This study was done to demonstrate the effects of Ephedrine HCL, Turmerone & Curcumin in Neurogenesis and Inhibition of Beta Amyloids in Transgenic Mice. The transgenic mice models used contain mutations associated with familial Alzheimer's disease (APP Swedish, MAPT P301L and PSEN1 M146V). These mice develop age-related, progressive neuropathology including plaques and tangles. Ten-month-old male and female APPSw Tg+ and Tgâ�� mice from 12 litters were randomly split between treatment groups. Tg+ mice were fed either chow containing a low dose of curcumin (160 ppm; n=9; a high dose of curcumin (5000 ppm; n=6), or no drug (n=8) for 6 months. Mice with low and high dose of curcumin were given specific doses of 0.02% Ephedrine HCL injection every 72 hours and underwent a single intracerebroventricular injection of 3 mg ar-turmerone. To evaluate whether curcumin treatment affected plaque pathology, cryostat hemibrain sections from Tg+ control and Tg+ low-dose curcumin-treated mice were immunostained with an antibody against A�²1â��13(DAE). Two-factor ANOVA revealed a significant reduction in plaque burden in curcumin, Ephedrine HCL and turmerone treated animals (F (1.60)=4.74; p=0.03), in which amyloid burden was decreased by 43.6% in treated animals compared with untreated animals. Soluble A�² in Tg+ untreated and Tg+ low-dose curcumin mice were measured by sandwich ELISA. Two-way ANOVA showed significant treatment effects in decreasing the levels of soluble A�² (*p<0.05). Underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via exon array analysis of cortical and hippocampal mRNA transcription showed a positive result.

Biography

Email: keerthiparamasivam2938@gmail.com