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加里森衰老研究所:老年个体及阿尔茨海默病患者的新希望。

Garrison Institute on Aging: A New Hope for Elderly Individuals and Patients with Alzheimer's Disease.

作者信息

Reddy P Hemachandra, Blackmon Joan, Molinar-Lopez Veronica, Ament Clay, Manczak Maria, Kandimalla Ramesh, Yin Xianglin, Pandey Akhilesh, Kuruva Chandra Sekhar, Wang Rui, Fry David, Osborn Carrah, Stonum Kathleen, Quesada Kandi, Gonzales Ruben, Boles Annette

机构信息

Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.

Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.

出版信息

J Alzheimers Dis. 2015;48(2):547-55. doi: 10.3233/JAD-150490.

DOI:10.3233/JAD-150490
PMID:26402018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5343754/
Abstract

The Garrison Institute on Aging (GIA) is an established institute within Texas Tech University Health Sciences Center, whose mission is to promote healthy aging through cutting-edge research on Alzheimer's disease (AD) and other diseases of aging through innovative educational opportunities for students, clinicians, researchers, health care professionals, and the public. The GIA has multiple programs, including both research and education on healthy aging and AD, community outreach, caregiving, the Retired Senior Volunteer Program, Healthy Lubbock, the GIA Brain Bank, healthy aging seminars, research seminars, and collaborations and scholarships. The GIA programs connect basic and clinical researchers and health care professionals, and provide a unique environment to help our growing elderly population and patients with AD and their families.

摘要

驻军老龄化研究所(GIA)是德克萨斯理工大学健康科学中心内的一个既定机构,其使命是通过对阿尔茨海默病(AD)和其他衰老疾病进行前沿研究,以及为学生、临床医生、研究人员、医疗保健专业人员和公众提供创新教育机会,来促进健康老龄化。GIA有多个项目,包括健康老龄化和AD的研究与教育、社区外展、护理、退休高级志愿者项目、健康拉伯克、GIA脑库、健康老龄化研讨会、研究研讨会以及合作与奖学金。GIA的项目将基础和临床研究人员以及医疗保健专业人员联系起来,并提供一个独特的环境来帮助不断增加的老年人群体以及AD患者及其家庭。

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引用本文的文献

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Garrison Institute on Aging-Lubbock Retired and Senior Volunteer Program (RSVP) Provides Services to South Plains, Texas.加里森衰老研究所-拉伯克退休及老年志愿者项目(RSVP)为得克萨斯州南平原地区提供服务。
Front Aging Neurosci. 2015 Dec 8;7:215. doi: 10.3389/fnagi.2015.00215. eCollection 2015.

本文引用的文献

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Increased mitochondrial fission and neuronal dysfunction in Huntington's disease: implications for molecular inhibitors of excessive mitochondrial fission.亨廷顿舞蹈病中线粒体裂变增加与神经元功能障碍:对过度线粒体裂变分子抑制剂的启示
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MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.线粒体靶向抗氧化剂MitoQ可延缓多发性硬化症实验性自身免疫性脑脊髓炎小鼠模型的疾病进展并减轻发病机制。
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Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's disease.阿尔茨海默病中线粒体功能障碍是由于 VDAC1 与淀粉样β和磷酸化 tau 的异常相互作用引起的。
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Mitochondria-targeted catalase reduces abnormal APP processing, amyloid β production and BACE1 in a mouse model of Alzheimer's disease: implications for neuroprotection and lifespan extension.线粒体靶向过氧化氢酶可减少阿尔茨海默病小鼠模型中异常 APP 加工、淀粉样 β 产生和 BACE1:对神经保护和延长寿命的影响。
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Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons: implications for mitochondrial dysfunction and neuronal damage.阿尔茨海默病神经元中线粒体裂变蛋白 Drp1 与过度磷酸化 tau 之间的异常相互作用:对线粒体功能障碍和神经元损伤的影响。
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Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's disease.突变型亨廷顿蛋白与线粒体蛋白 Drp1 的相互作用会损害线粒体生物发生,导致亨廷顿病中的轴突运输缺陷和突触退化。
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