Sajad Mohd, Kumar Rajesh, Thakur Sonu Chand
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.
Department of Reproductive Bio-medicine, The National Institute of Health and Family Welfare, Baba Gang Nath Marg, Munirka, New Delhi 110067, India.
IBRO Neurosci Rep. 2022 Apr 28;12:377-389. doi: 10.1016/j.ibneur.2022.04.009. eCollection 2022 Jun.
Alzheimer's disease is a steadily progressive, irreversible neurological disorder that is most frequently categorized under the umbrella term "neurodegeneration". Several attempts are underway to clarify the pathogenic mechanisms, identify the aetiologies, and determine a pathway by which the therapeutic steps can be implemented. Oxidative stress is one of the pathogenic processes, which is commonly believed to be associated with neurodegenerative diseases. Accumulation of extracellular amyloid-β protein (Aβ), hyperphosphorylation of tau, initiation of neurometabolic reactions characterized by the loss of neuronal function and synaptic failure, and decreased or lost learning capability and memory function are the most central neuropathological characteristics of AD. According to the amyloid cascade hypothesis, the enhanced deposition of Aβ deposits and neurofibrillary tangles due to hyperphosphorylation of Tau activates the cascade reactions in the brain. These reactions affect the synaptic activity and activation of microglia, which results in neuroinflammation due to enhanced immune function. Plant-based phytochemicals have also been used long ago against several diseases. Phytoconstituents play a significant neuroprotective property by preventing the pathophysiology of the disease. In this review, we have discussed the formation and crosstalk between amyloid and tau pathologies as well as the effect of neuroinflammation on the progression of AD. We have specifically focused on the formation of NFT, β-amyloids, inflammation, and pathophysiology of AD and the role of phytochemicals in the prevention of AD.
阿尔茨海默病是一种持续进展、不可逆转的神经退行性疾病，最常归类于“神经退行性变”这一统称之下。目前正在进行多项尝试，以阐明其致病机制、确定病因，并找到一条能够实施治疗步骤的途径。氧化应激是致病过程之一，通常被认为与神经退行性疾病有关。细胞外淀粉样β蛋白（Aβ）的积累、tau蛋白的过度磷酸化、以神经元功能丧失和突触功能障碍为特征的神经代谢反应的启动，以及学习能力和记忆功能的减退或丧失，是阿尔茨海默病最核心的神经病理学特征。根据淀粉样蛋白级联假说，由于Tau蛋白过度磷酸化导致的Aβ沉积物和神经原纤维缠结的沉积增加，激活了大脑中的级联反应。这些反应影响突触活动和小胶质细胞的激活，进而由于免疫功能增强导致神经炎症。基于植物的植物化学物质很久以前就被用于对抗多种疾病。植物成分通过预防疾病的病理生理学发挥显著的神经保护特性。在这篇综述中，我们讨论了淀粉样蛋白和tau蛋白病理之间的形成和相互作用，以及神经炎症对阿尔茨海默病进展的影响。我们特别关注了神经原纤维缠结、β淀粉样蛋白、炎症和阿尔茨海默病的病理生理学的形成，以及植物化学物质在预防阿尔茨海默病中的作用。
