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Garrison Institute on Aging: A New Hope for Elderly Individuals and Patients with Alzheimer's Disease.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。
J Alzheimers Dis. 2015;48(2):547-55. doi: 10.3233/JAD-150490.
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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.
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Design of comprehensive Alzheimer's disease centers to address unmet national needs.设计综合性阿尔茨海默病中心，以满足未满足的国家需求。
Alzheimers Dement. 2010 Mar;6(2):150-5. doi: 10.1016/j.jalz.2009.11.004.
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Current Status of Healthy Aging and Dementia Research: A Symposium Summary.健康老龄化与痴呆症研究现状：研讨会综述。
J Alzheimers Dis. 2019;72(s1):S11-S35. doi: 10.3233/JAD-190252.
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Japan as the front-runner of super-aged societies: Perspectives from medicine and medical care in Japan.日本作为超老龄化社会的领跑者：来自日本医学与医疗护理的视角
Geriatr Gerontol Int. 2015 Jun;15(6):673-87. doi: 10.1111/ggi.12450. Epub 2015 Feb 5.
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Keeping Lubbock healthy.
Tex Med. 2012 Jan 1;108(1):39-43.
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Workshop on Synergies Between Alzheimer's Research and Clinical Gerontology and Geriatrics: Current Status and Future Directions.阿尔茨海默病研究与临床老年医学和老年病学之间协同作用研讨会：现状与未来方向。
J Gerontol A Biol Sci Med Sci. 2018 Aug 10;73(9):1229-1237. doi: 10.1093/gerona/gly041.
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Lifestyle and Risk Factors of Dementia in Rural West Texas.德克萨斯州西部农村地区痴呆的生活方式和危险因素。
J Alzheimers Dis. 2019;72(s1):S1-S10. doi: 10.3233/JAD-191280.
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Commentary on "a roadmap for the prevention of dementia II. Leon Thal Symposium 2008." Centers of excellence in Alzheimer's disease: it is time to better integrate patient care and clinical research to improve the prevention and treatment of Alzheimer's disease.关于《预防痴呆症路线图II. 2008年莱昂·索尔研讨会》的评论。阿尔茨海默病卓越中心：是时候更好地整合患者护理与临床研究，以改善阿尔茨海默病的预防和治疗了。
Alzheimers Dement. 2009 Mar;5(2):133-6. doi: 10.1016/j.jalz.2009.01.006.
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The Toulouse Gérontopôle Research Center: report of activities, 2007-2011.《图卢兹老年医学研究中心活动报告，2007-2011》。
J Alzheimers Dis. 2012;28(3):721-32. doi: 10.3233/JAD-2011-112202.
引用本文的文献
1
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
Drug Discov Today. 2014 Jul;19(7):951-5. doi: 10.1016/j.drudis.2014.03.020. Epub 2014 Mar 28.
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Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction.线粒体分裂抑制剂作为治疗氧化应激和线粒体功能障碍相关疾病的一种策略。
J Alzheimers Dis. 2014;40(2):245-56. doi: 10.3233/JAD-132060.
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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。
Biochim Biophys Acta. 2013 Dec;1832(12):2322-31. doi: 10.1016/j.bbadis.2013.09.005. Epub 2013 Sep 19.
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Abnormal interaction of oligomeric amyloid-β with phosphorylated tau: implications to synaptic dysfunction and neuronal damage.寡聚态淀粉样-β与磷酸化 tau 异常相互作用：对突触功能障碍和神经元损伤的影响。
J Alzheimers Dis. 2013;36(2):285-95. doi: 10.3233/JAD-130275.
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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。
Hum Mol Genet. 2012 Dec 1;21(23):5131-46. doi: 10.1093/hmg/dds360. Epub 2012 Aug 27.
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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。
Hum Mol Genet. 2012 Jul 1;21(13):2973-90. doi: 10.1093/hmg/dds128. Epub 2012 Apr 5.
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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。
Hum Mol Genet. 2012 Jun 1;21(11):2538-47. doi: 10.1093/hmg/dds072. Epub 2012 Feb 24.
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Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's disease.突变型亨廷顿蛋白、异常的线粒体动力学、线粒体轴突运输缺陷以及亨廷顿病中的选择性突触退化。
Biochim Biophys Acta. 2012 Feb;1822(2):101-10. doi: 10.1016/j.bbadis.2011.10.016. Epub 2011 Nov 4.
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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。
Hum Mol Genet. 2012 Jan 15;21(2):406-20. doi: 10.1093/hmg/ddr475. Epub 2011 Oct 13.
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Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage.阿尔茨海默病患者神经元中线粒体动力学受损和淀粉样β蛋白与线粒体蛋白 Drp1 异常相互作用：对神经元损伤的影响。
Hum Mol Genet. 2011 Jul 1;20(13):2495-509. doi: 10.1093/hmg/ddr139. Epub 2011 Mar 31.
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