Altered expression of a-type but not b-type synapsin isoform in the brain of patients at high risk for Alzheimer's disease assessed by DNA microarray technique

被引:98
作者
Ho, L
Guo, YJ
Spielman, L
Petrescu, O
Haroutunian, V
Purohit, D
Czernik, A
Yemul, S
Aisen, PS
Mohs, R
Pasinetti, GM
机构
[1] Mt Sinai Sch Med, Neuroinflammat Res Labs, Dept Psychiat, New York, NY 10029 USA
[2] Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA
[3] Rockefeller Univ, Mol & Cellular Neurosci Lab, New York, NY 10021 USA
关键词
Alzheimer's disease; microarrays; synapsin; clinical dementia;
D O I
10.1016/S0304-3940(00)01753-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Using a cDNA microarray representing 6794 distinct human genes, we identified candidate genes whose expression is altered in cerebral cortex of cases of early Alzheimer's disease (AD); among these was the synaptic vesicle protein synapsin II, which plays an important role in neurotransmitter release. While other candidate genes are presently under investigation in our lab, in this study we discuss the regulation of synapsin gene expression during the transition from normal cognitive function to early AD. We found a selective decrease in the expression of the synapsin splice variants I-III of the a-type isoform in the entorhinal (EC, BM36) but not visual cortex (VC, BM17) of cases characterized by the earliest clinically detectable stage of AD. In contrast, we found no changes in synapsin splice variant II of the b-type isoform. Alteration of synapsin expression at the earliest clinical stage of AD may suggest novel strategies for improved treatment. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:191 / 194
页数:4
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