摘要
阿尔茨海默病是老年人中最常见的痴呆形式。但是,其发生、发展的发病机制只是被部分的了解。至今,收集到的临床和实验证据表明蓝斑,脑中去甲肾上腺素的主要来源,代表着病理的“中心”,其导致了AD的发展。这样的证据包括了LC调控的几个过程,且在AD患者脑中发生了改变的观察结果,包括突触可塑性、神经炎症、神经元代谢和血脑屏障的渗透性。而且,在AD患者的脑中LC经历了显著的退化,其被认为是由LC的去甲肾上腺素神经元,对前脑结构的刺激的tau蛋白病理性类阮病毒传播的来源。此外,由LC损伤增重AD相关的病理,而增强大脑的去神经传递减低了神经炎症和认知的减退。我们假设更好的理解LC神经元在AD发病机制中的作用可能导致新的治疗AD的策略的发展。
关键词: 阿尔茨海默病,血脑屏障,蓝斑,神经炎症,适应性,tau蛋白
Current Alzheimer Research
Title:Locus (Coeruleus) Minoris Resistentiae in Pathogenesis of Alzheimer’s Disease
Volume: 11 Issue: 10
Author(s): Boris Mravec, Katarina Lejavova and Veronika Cubinkova
Affiliation:
关键词: 阿尔茨海默病,血脑屏障,蓝斑,神经炎症,适应性,tau蛋白
摘要: Alzheimer’s disease (AD) represents the most prevalent form of dementia in the elderly. However, the pathological mechanisms underlying the development and progression of AD are only partially understood. To date, the accumulated clinical and experimental evidence indicate that the locus coeruleus (LC), the main source of brain’s norepinephrine, represents “the epicenter” of pathology leading to the development of AD. Evidence for this includes observations that neurons of the LC modulate several processes that are altered in brains of AD patients, including synaptic plasticity, neuroinflammation, neuronal metabolism, and blood-brain-barrier permeability. Moreover, the LC undergoes significant degeneration in the brains of AD patients and is considered a source of the prion-like spreading of tau pathology to forebrain structures innervated by the noradrenergic neurons of the LC. Furthermore, lesions of the LC exaggerate AD-related pathology, while augmentation of the brain’s noradrenergic neurotransmission reduces both neuroinflammation and cognitive decline. We hypothesize that better understanding the role of the LC neurons in AD pathogenesis may lead to development of new strategies for the treatment of AD.
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Boris Mravec, Katarina Lejavova and Cubinkova Veronika, Locus (Coeruleus) Minoris Resistentiae in Pathogenesis of Alzheimer’s Disease, Current Alzheimer Research 2014; 11 (10) . https://dx.doi.org/10.2174/1567205011666141107130505
DOI https://dx.doi.org/10.2174/1567205011666141107130505 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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