分析小胶质细胞引发的微囊泡,发掘其作为诊断阿尔茨海默病的有效可预见生物标记物的潜伏潜力:系统综述。

IF 2.3 4区 医学 Q3 CLINICAL NEUROLOGY
Brain Circulation Pub Date : 2024-09-26 eCollection Date: 2024-07-01 DOI:10.4103/bc.bc_113_23
Sri Harsha Kanuri, Prapthi Jayesh Sirrkay
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引用次数: 0

摘要

背景:阿尔茨海默病是一种神经退行性疾病,其特征是老年人脑组织中磷酸化 tau 和淀粉样蛋白沉积物的积累。假设:缺氧、氧化应激和炎症是神经元环境中常见的危险因素,它们会破坏神经元与突触之间的相互作用,并导致神经元凋亡。神经元凋亡的一个附带结果是小胶质细胞活化,它在启动先天性免疫防御系统以抵御和逆转所遇到的毒性刺激方面发挥着重要作用:结果:在这种情况下,小胶质细胞活化的一个潜在后果是组装、加工微囊并将其渗入细胞外空间。这些微囊会与淀粉样蛋白和 tau 沉积物包装在一起,而淀粉样蛋白和 tau 沉积物会在小胶质细胞内积聚,这是因为它们具有专业的清除功能。这些小胶质细胞微囊容易将 tau 和淀粉样蛋白 beta 种子播撒到周围的神经元突触框架中,因此与 AD 疾病病理的扩散有关:因此,在临床 AD 群体中,这些微粒胶质细胞可被视为疾病开始、发展、监测以及衡量治疗反应的预兆。我们推测未来的研究将揭示这些小胶质细胞 MV 的休眠潜能,并将其作为诊断、评估 AD 疾病进展和治疗的可靠标记物。这将为AD的早期诊断打开一扇大门,从而确定管理的优先次序并优化临床结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Profiling of microglial-originated microvesicles to unearthing their lurking potential as potent foreseeable biomarkers for the diagnosis of Alzheimer's disease: A systematic review.

Background: Alzheimer's Disease is a neurodegenerative disease characterized by accumulation of phosphorylated tau and amyloid deposits within the brain tissues in the elderly population. Numerous studies established that amassment of these toxic accretions within the brain tissues initiates neuronal demise and synaptic impairment which becomes the underlying basis for memory loss and cognitive abnormalities in these patients.

Hypothesis: Hypoxia, oxidative stress, and inflammation are commonly encountered perils in the neuronal milieu that derail the neuron-synapse interactions and maneuver them to undergo apoptosis. A spinoff from neuronal desecration is microglial activation which forms a cardinal role in mounting innate immune defenses for warding off and reversing off toxic stimulus encountered.

Results: A potential ramification of microglial activation in this context is assembly, processing and exuding of micro-vesicles into the extracellular space. These micro-vesicles will be packaged with amyloid and tau deposits which accumulate intracellularly within microglial cells secondary to their professional scavenging function. These microglial MVs are prone to seed tau and amyloid beta into the surrounding neuron-synapse framework, thus are implicated in spreading the disease pathology in AD.

Conclusions: Therefore, these MVs can be considered as an omen for disease initiation, progression, monitoring as well gauging the treatment response in the clinical AD cohorts. We speculate future research studies to unmask the dormant potential of these microglial MVs as reliable markers for diagnosis, evaluating the disease progression as well as treatment in AD. This will open the door for early diagnosis of AD so as to prioritize management and optimize clinical outcomes..

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Brain Circulation
Brain Circulation Multiple-
自引率
5.30%
发文量
31
审稿时长
16 weeks
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