阿尔茨海默病进展的病理生理机制及其相互关系的系统评估

S. Mittal, Akriti Sharma, Gauri Mittal, Ashwini A Mahadule, Monica Pathania
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引用次数: 0

摘要

阿尔茨海默病(AD)占所有痴呆病例的60-80%,因此被认为是最常见的痴呆形式。目前,阿尔茨海默病领域的临床医生和研究人员面临的挑战是制定能够在分子水平上针对病理进展的治疗方案,以及更新的诊断技术,以早期发现和预防阿尔茨海默病。这可以通过增强我们对阿尔茨海默病潜在病理生理学的理解来实现。这是系统和简明的各种病理生理机制,有助于AD的审查。本文采用合法的索引门户和检索网站进行文献检索。使用了MeSH术语和布尔运算符的组合。首先通过阅读标题和摘要,最后通过阅读全文来仔细评估获得的研究文章。采用一套纳入和排除标准来选择参考文献。在我们的文献检索中,在删除重复记录后,从PubMed、Google scholar和Cochrane Library中获得了75篇文献。使用标题和摘要对这些内容进行筛选。根据排除标准,23篇文章被排除在研究之外。阅读了52篇文章的全文。在撰写本综述的过程中,我们排除了7篇文章,仔细研究了45篇,引用了30篇。老年、糖尿病、吸烟、基因突变等各种风险因素会导致α和γ分泌酶裂解APP蛋白,从而导致β斑块积聚。Aβ斑块进一步促进神经原纤维缠结的积累、神经炎症和氧化应激。这与钙稳态紊乱和谷氨酸受体兴奋性毒性一起导致神经变性和突触毒性。
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Systematic assessment of pathophysiological mechanisms and their interrelation in progression of Alzheimer’s disease
Alzheimer’s disease (AD) consists of 60-80% of all dementia cases, thus is recognized as the commonest form of dementia. The current challenge to clinicians and researchers in the field of AD is development of treatment plans that can target the progression of pathology at molecular level as well newer diagnostic techniques for early detection and prevention of AD. This could be achieved by enhancing our understanding of the underlying pathophysiology of AD. This is systematic and concise review of various pathophysiological mechanisms contributing to AD. Legitimate indexing portals and search websites were used to carry out the literature search for this article. A combination of MeSH terms and Boolean operators were used. Obtained research articles were carefully assessed first by reading title and abstract and finally by reading the whole text. A set of inclusion and exclusion criteria were used to select the reference articles.: In our literature search 75 articles were obtained from PubMed, Google scholar and Cochrane Library after removing duplicate records. These were screened using titles and abstract. 23 articles were excluded from the study as per the exclusion criteria. Full text of 52 articles were read. 7 articles were excluded, 45 were studied thoughrouly and 30 were referenced during the writing of this review.Various risk factors – old age, diabetes, smoking, mutation etc contribute to Aβ plaque accumulation due to cleavage of APP protein by α and ϒ secretase. Aβ plaque further contributes to accumulation of neurofibrillary tangles, neuroinflammation and oxidative stress. This together with disturbance in Calcium homeostasis and excitotoxicity at glutamate receptors contribute to neurodegeneration and synaptic toxicity.
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