Bhatti Gurjit Kaur, Reddy Arubala P, Reddy P Hemachandra, Bhatti Jasvinder Singh
Department of Medical Lab Technology, University Institute of Applied Health Sciences, Chandigarh University, Mohali, India.
Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
Front Aging Neurosci. 2020 Jan 10;11:369. doi: 10.3389/fnagi.2019.00369. eCollection 2019.
Alzheimer's disease (AD) is a type of incurable neurodegenerative disease that is characterized by the accumulation of amyloid-β (Aβ; plaques) and tau hyperphosphorylation as neurofibrillary tangles (NFTs) in the brain followed by neuronal death, cognitive decline, and memory loss. The high prevalence of AD in the developed world has become a major public health challenge associated with social and economic burdens on individuals and society. Due to there being limited options for early diagnosis and determining the exact pathophysiology of AD, finding effective therapeutic strategies has become a great challenge. Several possible risk factors associated with AD pathology have been identified; however, their roles are still inconclusive. Recent clinical trials of the drugs targeting Aβ and tau have failed to find a cure for the AD pathology. Therefore, effective preventive strategies should be followed to reduce the exponential increase in the prevalence of cognitive decline and dementia, especially AD. Although the search for new therapeutic targets is a great challenge for the scientific community, the roles of lifestyle interventions and nutraceuticals in the prevention of many metabolic and neurodegenerative diseases are highly appreciated in the literature. In this article, we summarize the molecular mechanisms involved in AD pathology and the possible ameliorative action of lifestyle and nutritional interventions including diet, exercise, Calorie restriction (CR), and various bioactive compounds on cognitive decline and dementia. This article will provide insights into the role of non-pharmacologic interventions in the modulation of AD pathology, which may offer the benefit of improving quality of life by reducing cognitive decline and incident AD.
阿尔茨海默病（AD）是一种无法治愈的神经退行性疾病，其特征是大脑中淀粉样蛋白-β（Aβ；斑块）的积累和tau蛋白过度磷酸化形成神经原纤维缠结（NFTs），随后导致神经元死亡、认知能力下降和记忆丧失。AD在发达国家的高发病率已成为一项重大的公共卫生挑战，给个人和社会带来了社会和经济负担。由于AD的早期诊断和确切病理生理学的确定方法有限，寻找有效的治疗策略已成为一项巨大的挑战。已经确定了几种与AD病理相关的可能风险因素；然而，它们的作用仍不明确。最近针对Aβ和tau的药物临床试验未能找到治愈AD病理的方法。因此，应采取有效的预防策略，以减少认知能力下降和痴呆症，尤其是AD发病率的指数级增长。尽管寻找新的治疗靶点对科学界来说是一项巨大的挑战，但生活方式干预和营养保健品在预防许多代谢性和神经退行性疾病中的作用在文献中得到了高度认可。在本文中，我们总结了AD病理所涉及的分子机制，以及生活方式和营养干预（包括饮食、运动、热量限制（CR）和各种生物活性化合物）对认知能力下降和痴呆症可能的改善作用。本文将深入探讨非药物干预在调节AD病理中的作用，这可能通过减少认知能力下降和AD发病率来提高生活质量。
