Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer's disease

被引：319

作者：

Gouras, Gunnar K. ^{[1
]}

Tampellini, Davide ^{[1
]}

Takahashi, Reisuke H. ^{[2
]}

Capetillo-Zarate, Estibaliz ^{[1
]}

机构：

[1] Weill Cornell Med Coll, Dept Neurol & Neurosci, New York, NY 10065 USA

[2] Tokyo Med Univ Hosp, Dept Pathol, Tokyo, Japan

来源：

ACTA NEUROPATHOLOGICA | 2010年 / 119卷 / 05期

基金：

美国国家卫生研究院;

关键词：

Amyloid; Synapse; Tau; Head injury; Endosome; Dementia pugilistica; INTRACELLULAR A-BETA; HEREDITARY CEREBRAL-HEMORRHAGE; TRANSGENIC MOUSE MODEL; PRECURSOR-PROTEIN; NEUROFIBRILLARY TANGLES; APOLIPOPROTEIN-E; PLAQUE-FORMATION; HEAD-INJURY; NEURON LOSS; MITOCHONDRIAL DYSFUNCTION;

D O I：

10.1007/s00401-010-0679-9

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The aberrant accumulation of aggregated beta-amyloid peptides (A beta) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of A beta has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby A beta is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular A beta have been viewed as the most important pathogenic form of A beta in AD. More recently, the intraneuronal accumulation of A beta 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 A beta accumulation to the development of synaptic pathology and plaques in AD, and discuss the implications of intraneuronal beta-amyloid for AD pathology, biology, diagnosis and therapy.

引用

页码：523 / 541

页数：19

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