摘要
背景:阿尔茨海默病(AD)是一种最常见的痴呆症,它是一种与分子、生理、解剖、生物标记物和认知维度相关的进展性神经退行性疾病。方法:本文对潜在阿尔茨海默病的生物变化(遗传、分子和细胞)和其与临床综合征的关系进行综述。结果:与阿尔茨海默病相关的痴呆症与β-淀粉样蛋白和tau蛋白的异常沉积、加工和清除有关。脑内β-淀粉样蛋白沉积在基底皮质开始并向不同的空间发展,蔓延整个海马,并最终蔓延大脑皮质的其他部分。通过神经网络传播的tau蛋白异常导致神经原纤维缠结明显一致的空间发展,从横嗅皮质和海马区开始和从上横向传播至新皮层。突触功能障碍和细胞死亡通过葡萄糖和进展性脑萎缩脑代谢率的逐步丧失而表现出来。海马齿状回突触数量减少与认知功能下降有关。淀粉样蛋白的变化可从脑脊液和通过淀粉样蛋白在发病前20年的影像学检查中检测到。通过磁共振成像,在临床症状出现10年之前便可检测到结构萎缩。结论:本文强调了阿尔茨海默潜在病患者的生物变化(遗传、分子和细胞)和它们与临床综合征的相关关系进行综述。在明显的症状出现之前,许多变化的发生是明显的,生物标志物提供了一种手段来检测阿尔茨海默病,即使患者没有出现该症状。
关键词: 阿尔茨海默病,解剖学,生物标志物,认知,分子,神经生物学,生理。
Current Alzheimer Research
Title:Neurobiology of Alzheimer’s Disease: Integrated Molecular, Physiological, Anatomical, Biomarker, and Cognitive Dimensions
Volume: 12 Issue: 8
Author(s): Joel Raskin, Jeffrey Cummings, John Hardy, Kory Schuh and Robert A. Dean
Affiliation:
关键词: 阿尔茨海默病,解剖学,生物标志物,认知,分子,神经生物学,生理。
摘要: Background: Alzheimer’s disease (AD), the most common form of dementia, is a progressive neurodegenerative disorder with interrelated molecular, physiological, anatomical, biomarker, and cognitive dimensions. Methods: This article reviews the biological changes (genetic, molecular, and cellular) underlying AD and their correlation with the clinical syndrome. Results: Dementia associated with AD is related to the aberrant production, processing, and clearance of beta-amyloid and tau. Beta-amyloid deposition in brain follows a distinct spatial progression starting in the basal neocortex, spreading throughout the hippocampus, and eventually spreading to the rest of the cortex. The spread of tau pathology through neural networks leads to a distinct and consistent spatial progression of neurofibrillary tangles, beginning in the transentorhinal and hippocampal region and spreading superolaterally to the primary areas of the neocortex. Synaptic dysfunction and cell death is shown by progressive loss of cerebral metabolic rate for glucose and progressive brain atrophy. Decreases in synapse number in the dentate gyrus of the hippocampus correlate with declining cognitive function. Amyloid changes are detectable in cerebrospinal fluid and with amyloid imaging up to 20 years prior to the onset of symptoms. Structural atrophy may be detectable via magnetic resonance imaging up to 10 years before clinical signs appear. Conclusion: This review highlights the progression of biological changes underlying AD and their association with the clinical syndrome. Many changes occur before overt symptoms are evident and biomarkers provide a means to detect AD pathology even in patients without symptoms.
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Raskin Joel, Cummings Jeffrey, Hardy John, Schuh Kory and Dean A. Robert, Neurobiology of Alzheimer’s Disease: Integrated Molecular, Physiological, Anatomical, Biomarker, and Cognitive Dimensions, Current Alzheimer Research 2015; 12 (8) . https://dx.doi.org/10.2174/1567205012666150701103107
DOI https://dx.doi.org/10.2174/1567205012666150701103107 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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