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Lifespan Modulation in Mice and the Confounding Effects of Genetic Background

Journal of Genetics and Genomics 2014年第9期41卷 497-503页

作者： Lorna Mulvey Amy Sinclair Colin Selman Institute of Biodiversity Animal Health and Comparative MedicineCollege of MedicineVeterinary and Life SciencesGraham Kerr BuildingUniversity of Glasgow

We are currently in the midst of a revolution in ageing research, with several dietary, genetic and pharmacological interventions now known to modulate ageing in model organisms. Excitingly, these interventions also appear to have beneficial effects on late-life health. For example, dietary restriction （DR） has been shown to slow the incidence of age-associated cardiovascular disease, metabolic disease, cancer and brain ageing in non-human primates and has been shown to improve a range of health indices in humans. While the idea thai DR＇s ability to extend lifespan is often thought of as being universal, studies in a range of organisms, including yeast, mice and monkeys, suggest that this may not actually be the case. The precise reasons underlying these differential effects of DR on lifespan are currently unclear, but genetic background may be an important factor in how an individual responds to DR. Similarly, recent findings also suggest that the responsiveness of mice to specific genetic or pharmacological interventions that modulate ageing may again be influenced by genetic background. Consequently, while there is a clear driver to develop interventions to improve late-life health and vitality, under- standing precisely how these act in response to particular genotypes is critical if we are to translate these findings to humans. We will consider of the role of genetic background in the efficacy of various lifespan interventions and discuss potential routes of utilising genetic heterogeneity to further understand how particular interventions modulate lifespan and healthspan.

关键词： Ageing dietary restriction Genotype Longevity

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Telomerase and mTOR in the brain:the mitochondria connection

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Neural Regeneration Research 2017年第3期12卷 358-361页

作者： Satomi Miwa Gabriele Saretzki Ageing Biology Centre and Institute for Cell and Molecular Biosciences Campus for Ageing and VitalityNewcastle UniversityNewcastle upon TyneUK

Telomerase is an enzyme that maintains telomeres in dividing cells using a template on its inherent RNA ***,the protein part TERT（Telomerase Reverse Transcriptase） has various non-canonical *** example,it can localize to mitochondria under increased stress and protect cells in vitro from oxidative stress,DNA damage and *** it has been demonstrated that TERT protein persists in adult neurons in the brain and data emerge suggesting that it might have a protective function in these post-mitotic cells as *** have recently published that TERT protein accumulated in mitochondria from brain tissue of mice that have undergone short-term dietary restriction（DR） and rapamycin *** localization correlated to lower levels of oxidative stress in these brain *** rapamycin treatment decreases mTOR signaling which is also thought to play an important role for the beneficial effects of DR,we conclude that the mTOR pathway might be involved in the TERT localization and its effects in brain mitochondria in *** data are in line with previous findings from our group about increased mitochondrial localization of TERT in Alzheimer＇s disease（AD） brains and a protective function of TERT protein in neurons in vitro against pathological tau.

关键词： telomerase brain neuron mitochondria roTOR ROS dietary restriction rapamycin

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