Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease.
Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease.
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DOI：
10.1007/s00401-010-0679-9
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发表时间：
2010-05
影响因子：
12.7
通讯作者：
Capetillo-Zarate E
中科院分区：
文献类型：
--
作者：
Gouras GK;Tampellini D;Takahashi RH;Capetillo-Zarate E
聚集的β-淀粉样多肽(A-β)以斑块的形式异常聚集是阿尔茨海默病(AD)神经病理的特征，减少A-β已成为该疾病实验治疗的主要方向。Aβ参与该病病理生理的机制(S)仍然知之甚少(S)。最初的纤维和随后的细胞外Aβ的寡聚体被认为是AD中Aβ的最重要的致病形式。最近，Aβ在大脑中的神经元内积累已被描述，尽管技术考虑及其与AD的相关性使这一问题成为一个有争议的话题。本文综述了神经元内A-β积聚与AD突触病理和斑块形成的关系，并讨论了神经元内β-淀粉样蛋白在AD病理、生物学、诊断和治疗中的意义。
The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer’s disease (AD) neuropathology and reduction of Aβ has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular Aβ have been viewed as the most important pathogenic form of Aβ in AD. More recently, the intraneuronal accumulation of Aβ has been described in the brain, although technical considerations and its relevance in AD have made this a controversial topic. Here we review the emerging evidence linking intraneuronal Aβ accumulation to the development of synaptic pathology and plaques in AD, and discuss the implications of intraneuronal β-amyloid for AD pathology, biology, diagnosis and therapy.
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