Neurophysiology unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand.
Neurophysiology unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai, 50200, Thailand.
Exp Gerontol. 2018 Jan;101:13-36. doi: 10.1016/j.exger.2017.10.029. Epub 2017 Nov 10.
Aging is a phenomenon that all living organisms inevitably face. Every year, 9.9million people, globally, suffer from dementia, an indicator of the aging brain. Brain aging is significantly associated with mitochondrial dysfunction. This is characterized by a decrease in the activity of respiratory chain enzymes and ATP production, and increased free radical generation, mitochondrial deoxyribonucleic acid (DNA) mutations, and impaired mitochondrial structures. To get a better understanding of aging and to prevent its effects on many organs, chronic systemic administration of D-galactose was used to artificially create brain senescence in animal models and established to be beneficial for studies of anti-aging therapeutic interventions. Several studies have shown that D-galactose-induced brain aging which does so not only by causing mitochondrial dysfunction, but also by increasing oxidative stress, inflammation, and apoptosis, as well as lowering brain-derived neurotrophic factors. All of these defects finally lead to cognitive decline. Various therapeutic approaches which act on mitochondria and cognition were evaluated to assess their effectiveness in the battle to reverse brain aging. The aim of this article is to comprehensively summarize and discuss the underlying mechanisms involved in D-galactose-induced brain aging, particularly as regards alterations in brain mitochondria and cognitive function. In addition, the aim is to summarize the different therapeutic approaches which have been utilized to address D-galactose-induced brain aging.
衰老是所有生物体不可避免地面临的现象。每年，全球有 990 万人患有痴呆症，这是大脑衰老的一个指标。大脑衰老与线粒体功能障碍密切相关。其特征是呼吸链酶活性和 ATP 产生减少，自由基生成增加，线粒体脱氧核糖核酸 (DNA) 突变，以及线粒体结构受损。为了更好地了解衰老，并防止其对许多器官的影响，人们使用慢性全身给予半乳糖的方法在动物模型中人为地制造脑衰老，并建立了用于抗衰老治疗干预研究的方法。多项研究表明，半乳糖诱导的脑衰老不仅会导致线粒体功能障碍，还会增加氧化应激、炎症和细胞凋亡，并降低脑源性神经营养因子。所有这些缺陷最终都会导致认知能力下降。评估了针对线粒体和认知的各种治疗方法，以评估它们在逆转脑衰老方面的有效性。本文的目的是全面总结和讨论半乳糖诱导的脑衰老涉及的潜在机制，特别是关于大脑线粒体和认知功能的改变。此外，还总结了用于解决半乳糖诱导的脑衰老的不同治疗方法。
