Scientists at Shiga University publish research in Alzheimer disease
2007 NOV 19 -- Research findings, 'RB1CC1 insufficiency causes neuronal atrophy through mTOR signaling alteration and involved in the pathology of Alzheimer's diseases,' are discussed in a new report. "RB1-inducible Coiled-Coil 1 (RB1CC1) has been shown to be a novel tumor suppressor regulating RB1 expression. Neuronal abundance of RB1CC1 is reported to contribute to the non-proliferating enlarged cell phenotype through the maintenance of RB1 and mTOR," scientists in Japan report. "To clarify whether RB1CC1 insufficiency is involved in neuronal atrophy and Alzheimer's pathology, we investigated modifications of RB1CC1 as a possible cause of atrophy or death through the disturbance of mTOR signaling in Neuro-2a neuroblastoma cells. We also evaluated the correlation between RB1CC1 and mTOR signaling in a series of Alzheimer's brain tissues. Though RB1CC1 introduction enhanced neurite growth, RNAi-mediated knockdown of RB1CC1 or rapamycin treatment caused neurite atrophy and apoptosis due to mTOR signaling reduction in the differentiated Neuro-2a cells. Both TSC1 and RB1CC1 were equally functional and maintained mTOR signaling, indicated by phospho-S6 (Ser240/244) expression in 69% of Alzheimer's (9/13 cases) and 100% of normal brains (6/6 cases). However, scanty RB1CC1 expression, less than TSC1, caused phospho-S6 disappearance in 31% of Alzheimer's tissues (4/13 cases). These findings suggest that RB1CC1 insufficiency may result in mTOR signaling repression through unbalanced TSC1 abundance and may induce neuronal atrophy," wrote T. Chano and colleagues, Shiga University. The researchers concluded: "These observations may have implications for the pathogenesis of Alzheimer's disease." Chano and colleagues published their study in Brain Research (RB1CC1 insufficiency causes neuronal atrophy through mTOR signaling alteration and involved in the pathology of Alzheimer's diseases. Brain Research, 2007;1168():97-105). For additional information, contact T. Chano, Shiga University of Medical Science, Dept. of Clinical Laboratory Medicine, Shiga 520-2192, Japan. The publisher's contact information for the journal Brain Research is: Elsevier Science BV, PO Box 211, 1000 AE Amsterdam, Netherlands. Keywords: Japan, Alzheimer Disease, Atrophy, Brain Research, Neurology, Oncology, Tumor Suppression. This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2007, Pain & Central Nervous System Week via NewsRx.com.
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