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Titlebook: Brain Aging and Therapeutic Interventions; Mahendra K. Thakur,Suresh I.S. Rattan Book 2012 Springer Science+Business Media Dordrecht 2012

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Book 2012elopments in the field of neurodegenerative disorders and their therapeutic interventions. This book will be of much interest to pharmaceutical, nutrition and healthcare industry for an easy access to accurate and reliable information in the field of aging research and intervention..
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https://doi.org/10.1007/978-3-8348-8117-5remature senescence and progeria like phenotype. These studies have demonstrated that mortalin-mediated mitochondrial functions are not only the key factors in maintaining the continued proliferation of cancer cells but also the normal neuronal physiology. Lack of a functional mortalin leads to cancer cell death and neurodegenerative phenotype.
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https://doi.org/10.1007/978-3-8348-9007-8 on oxidative stress and cognitive decline with age on animal models and human subjects showing the importance of non-polyphenolic and polyphenolic-rich plant products in alleviating age-related cognitive loss.
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Consequences of Altered Mortalin Expression in Control of Cell Proliferation and Brain Function,remature senescence and progeria like phenotype. These studies have demonstrated that mortalin-mediated mitochondrial functions are not only the key factors in maintaining the continued proliferation of cancer cells but also the normal neuronal physiology. Lack of a functional mortalin leads to cancer cell death and neurodegenerative phenotype.
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Book 2012elated brain disorders. It includes 18 chapters by leading researchers, and each chapter is a comprehensive and critical review of the topic in question, discusses the current scenario and focuses on future perspectives. The target readership is the undergraduate and graduate students in the univers
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https://doi.org/10.1007/978-3-658-39516-2in maintaining the structural integrity of DNA that is quite often threatened from events taking place within the cell itself. Implicit in this crucial role is also the fact that any perturbation in this repair pathway could lead to deleterious consequences—particularly in a post-mitotic tissue like
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