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Moorthy, K., Yadav, U.C.S., Siddiqui, M.R., Mantha, A.K., Basir, S.F., Sharma, D., Cowsik, S.M. and Baquer, N.Z. (2005) Effect of hormone replacement therapy innormalizing age related neuronal markers in different age groups of naturally menopausal rats. Biogerontology, 6, 345-356. http://dx.doi.org/10.1007/s10522-005-4810-6

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• TITLE: Neuroprotective role of 17β estradiol with tachykinin neuropeptide NKB and Aβ (25 - 35) in aging female rat brain

  AUTHORS: Rashmi Jha, Abbas Ali Mahdi, Shivani Pandey, Najma Z. Baquer, Sudha M. Cowsik

  KEYWORDS: Neurokinin B; Amyloid Beta (25 - 35); Estradiol; Neurodegenerative Diseases

  JOURNAL NAME: Advances in Aging Research, Vol.2 No.4, October 10, 2013

  ABSTRACT: The brain experiences structural, molecular and functional alterations during aging. In aging brain tissue, the oxidative stress increases due to decreased activity of antioxidant enzymes and increased oxidative stress leading to neurodegeneration associated with excitotoxicity. In the present study, we observed the effect of tachykinin neuropeptide Neurokinin B (NKB) and amyloid beta fragment Aβ (25 -35) on the activity of Acetylcholine esterase (AChE) and Lipid peroxidation (LPO) in brains of 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. An in-vitro incubation of E2 treated brain synaptosomes with Aβ (25 -35) showed toxic effects on all the parameters. The treatment of NKB and combined NKB and Aβ (25 -35) increased the AChE enzyme activity and decreased the level of LPO in E2 treated aging rats. The treatment of NKB and combined NKB and Aβ (25 - 35) in a concentration dependent manner reversed the effects of aging and Aβ (25 -35) on AChE and LPO. The present finding suggests that E2 along with NKB reverse aging and Aβ (25 -35) induced toxicity as well as AChE and LPO levels. The results of the current study showed a possible beneficial role of NKB with E2 inthe age related neurological diseases.