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Calabrese, V., Cornelius, C., Mancuso, C., Pennisi, G., Calafato, S., Bellia, F., Bates, T.E., Giuffrida Stella, A.M., Schapira, T., DinkovaKostova, A.T. and Rizzarelli, E. (2008) Cellular Stress Response: A Novel Target for Chemoprevention and Nutritional Neuroprotectionin Aging, Neurodegenerative Disorders and Longevity. Neurochemical Research, 33, 2444-2471.
http://dx.doi.org/10.1007/s11064-008-9775-9

has been cited by the following article:

• TITLE: Therapeutic Potential of 17β Estradiol with Tachykinin Neuropeptide NKB and Aβ(25 - 35) on Na+ - K+ ATPase Activity in Aging Female Rat Brain

  AUTHORS: Rashmi Jha, Priyanka Mishra, Ranjeet Kumar, Abbas Ali Mahdi, Shivani Pandey, Najma Zaheer Baquer, Sudha Mahajan Cowsik

  KEYWORDS: Na+ - K+ ATPase, Aging, Neurokinin B, Amyloid Beta (25 - 35), Estradiol

  JOURNAL NAME: Advances in Aging Research, Vol.4 No.2, February 26, 2015

  ABSTRACT: The Na+ - K+ ATPase is an enzyme responsible for the active transport of Na+ and K+ in most eukaryotic cells. The aim of the present study was to determine the effect of Tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 - 35) on 17β estradiol (E2) treated aging female rat brain synaptosomes of different age groups, by assaying Na+ - K+ ATPase enzyme activity. An in vitro incubation of isolated synaptosomes with Aβ (25 - 35) showed toxic effects while NKB showed stimulating effect on the Na+ - K+ ATPase activity, and the combined NKB + Aβ (25 - 35) incubations showed a partial effect as compared to the Aβ (25 - 35) alone. To understand whether E2 affects the expression of Na+ - K+ ATPase molecules, we examined the expression of Na+ - K+ ATPase subunit α1 and β2 in E2 treated aging female rat brain synaptosomes. The enzyme was quantified by SDS PAGE in control and E2 treated rat brain. We observed that the expression of α1 and β2 Na+ - K+ ATPase molecules increased and reversed to a normal level in E2 treated synaptosomes. These results confirmed that E2 increased turnover of Na+ - K+ ATPase molecules in aging rat brain. The present findings also suggest a possible role of NKB with E2 in the age related changes in the brain.