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To: r.edwards who wrote (2591)	6/20/2000 10:56:00 PM
From: r.edwards	Respond to of 13572

Talking with a Neuro-Surgeon last Thursday at his house, I rarely get to use my biology any more but I brought up Gelera and Genron,,, He was hot on Telomerase as a link to Alzheimers and even Parkinsons................... Telomerase and Alzheimer's Disease by: elbarado_99 6/20/00 3:42 pm Msg: 28947 of 28959 We heard about this a few days ago...here's a link to the article: jneurochem.org This is great news for those suffering from Alzheimer's disease - and Geron's hTERT patents are right in the middle of it all. Journal of Neurochemistry, Vol. 75, No. 1, 2000 117-124 ¸ 2000 International Society for Neurochemistry The Catalytic Subunit of Telomerase Protects Neurons Against Amyloid á-Peptide-Induced Apoptosis Haiyan Zhu, Weiming Fu and Mark P. Mattson, Sanders-Brown Research Center on Aging, University of Kentucky, Lexington, Kentucky Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, U.S.A. Abstract : The catalytic subunit of telomerase (TERT) is a specialized reverse transcriptase that has been associated with cell immortalization and cancer. It was reported recently that TERT is expressed in neurons throughout the brain in embryonic and early postnatal development, but is absent from neurons in the adult brain. We now report that suppression of TERT levels and function in embryonic mouse hippocampal neurons in culture using antisense technology and the telomerase inhibitor 3' -azido-2' 3' -dideoxythymidine significantly increases their vulnerability to cell death induced by amyloid á-peptide, a neurotoxic protein believed to promote neuronal degeneration in Alzheimer's disease. Neurons in which TERT levels were reduced exhibited increased levels of oxidative stress and mitochondrial dysfunction following exposure to amyloid á-peptide. Overexpression of TERT in pheochromocytoma cells resulted in decreased vulnerability to amyloid á-peptide-induced apoptosis. Our findings demonstrate a neuroprotective function of TERT in an experimental model relevant to Alzheimer's disease, and suggest the possibility that restoration of TERT expression in neurons in the adult brain may protect against age-related neurodegeneration. --------------------------------------------------------------------------------