Department of Molecular and Integrative Physiology, The University of Kansas Medical Center, Kansas City, Kansas.
Department of Neurology, The University of Kansas Medical Center, Kansas City, Kansas.
J Appl Physiol (1985). 2020 Dec 1;129(6):1468-1476. doi: 10.1152/japplphysiol.00168.2020. Epub 2020 Sep 24.
Alzheimer's disease (AD) is the most common neurodegenerative disease, yet there are no disease-modifying treatments available and there is no cure. It is becoming apparent that metabolic and vascular conditions such as type 2 diabetes (T2D) and hypertension promote the development and accumulation of Alzheimer's disease-related dementia pathologies. To this end, aerobic exercise, which is a common lifestyle intervention for both metabolic disease and hypertension, is shown to improve brain health during both healthy aging and dementia. However, noncompliance or other barriers to exercise response are common in exercise treatment paradigms. In addition, reduced intracellular proteostasis and mitochondrial function could contribute to the etiology of AD. Specifically, compromised chaperone systems [i.e., heat shock protein (HSP) systems] can contribute to protein aggregates (i.e., β-amyloid plaques and neurofibrillary tangles) and reduced mitochondrial quality control (i.e., mitophagy). Therefore, novel therapies that target whole body metabolism, the vasculature, and chaperone systems (like HSPs) are needed to effectively treat AD. This review focuses on the role of heat therapy in the treatment and prevention of AD. Heat therapy has been independently shown to reduce whole body insulin resistance, improve vascular function, activate interorgan cross talk via endocytic vesicles, and activate HSPs to improve mitochondrial function and proteostasis in a variety of tissues. Thus, heat therapy could offer immense clinical benefit to patients suffering from AD. Importantly, future studies in patients are needed to determine the safety and efficacy of heat therapy in preventing AD.
阿尔茨海默病(AD)是最常见的神经退行性疾病,但目前尚无可改变疾病进程的治疗方法,也无法治愈。越来越明显的是,代谢和血管状况,如 2 型糖尿病(T2D)和高血压,会促进与阿尔茨海默病相关的痴呆病理的发展和积累。为此,有氧运动作为代谢疾病和高血压的常见生活方式干预措施,已被证明可以在健康衰老和痴呆期间改善大脑健康。然而,在运动治疗模式中,运动的不依从或其他障碍很常见。此外,细胞内蛋白质稳态和线粒体功能的降低可能是 AD 的病因之一。具体来说,伴侣蛋白系统(即热休克蛋白(HSP)系统)受损会导致蛋白质聚集(即β-淀粉样斑块和神经原纤维缠结)和线粒体质量控制降低(即自噬)。因此,需要针对全身代谢、血管和伴侣蛋白系统(如 HSP)的新型疗法来有效治疗 AD。本综述重点介绍热疗在 AD 的治疗和预防中的作用。热疗已被独立证明可降低全身胰岛素抵抗,改善血管功能,通过内吞小泡激活器官间的交流,并激活 HSP 以改善多种组织中的线粒体功能和蛋白质稳态。因此,热疗可能为 AD 患者带来巨大的临床益处。重要的是,需要在患者中进行未来的研究,以确定热疗预防 AD 的安全性和有效性。