Expression of beta-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila

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	Expression of beta-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila
	Huang, Fu-De
刊名	JOURNAL OF NEUROSCIENCE
	2010
卷号	30 期号:4 页码:1512-1522
关键词	LONG-TERM POTENTIATION IMPAIR SYNAPTIC PLASTICITY INTRANEURONAL-A-BETA ALZHEIMERS-DISEASE TRANSGENIC MICE PRECURSOR PROTEIN MITOCHONDRIAL DYSFUNCTION COGNITIVE DECLINE PLAQUE-FORMATION NEURODEGENERATIVE DISEASES
ISSN号	0270-6474
通讯作者	Huang, FD (reprint author), Chinese Acad Sci, Inst Neurosci, Shanghai Inst Biol Sci, 320 Yue Yang Rd, Shanghai 200031, Peoples R China,fdhuang@ion.ac.cn
英文摘要	Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature and progression of the presynaptic structural and functional changes in AD are essentially unknown. We expressed wild-type or arctic form of beta amyloid(1-42) (A beta) in a small group of neurons in the adult fly and performed extensive time course analysis of the function and structure of both axon and presynaptic terminals at the identified single-neuron level. A beta accumulated intracellularly and induced a range of age-dependent changes, including depletion of presynaptic mitochondria, slowdown of bi-directional transports of axonal mitochondria, decreased synaptic vesicles, increased large vacuoles, and elevated synaptic fatigue. These structural and functional synaptic changes correlated with age-dependent deficit in motor behavior. All these alterations were accelerated in flies expressing the arctic form of A beta. The depletion of presynaptic mitochondria was the earliest detected phenotype and was not caused by the change in axonal transport of mitochondria. Moreover, axonal mitochondria exhibited a dramatic reduction in number but a significant increase in size in aged A beta-expressing flies, indicating a global depletion of mitochondria in the neuron and an impairment of mitochondria fission. These results suggest that A beta accumulation depletes presynaptic and axonal mitochondria, leading to other presynaptic deficits.
学科主题	Neurosciences & Neurology
收录类别	SCI
资助信息	973 Program[2006CB806600, 2007CB947101]; Knowledge Innovation Engineering Project of the Chinese Academy of Sciences[KSCX2-YW-R-099]; Shanghai Municipal Program for Basic Research[06dj14010]
语种	英语
公开日期	2012-07-13
内容类型	期刊论文
源URL	[http://ir.sibs.ac.cn/handle/331001/1620]
专题	上海神经科学研究所_神经所(总) 上海神经科学研究所_神经退行性疾病研究小组
推荐引用方式 GB/T 7714	Huang, Fu-De. Expression of beta-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila[J]. JOURNAL OF NEUROSCIENCE,2010,30(4):1512-1522.
APA	Huang, Fu-De.(2010).Expression of beta-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila.JOURNAL OF NEUROSCIENCE,30(4),1512-1522.
MLA	Huang, Fu-De."Expression of beta-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila".JOURNAL OF NEUROSCIENCE 30.4(2010):1512-1522.