Connexins and pannexins in Alzheimer's disease

被引：23

作者：

Giaume, Christian ^{[1
]}

Saez, Juan C. ^{[2
,3
]}

Song, Weihong ^{[4
]}

Leybaert, Luc ^{[5
]}

Naus, Christian C. ^{[6
]}

机构：

[1] Coll France, ICIRB, CNRS, UMR7241,INSERM, Paris 05, France

[2] Pontificia Univ Catolica Chile, Dept Fisiol, Santiago, Chile

[3] Inst Milenio Neurociencias Valparaiso, Valparaiso, Chile

[4] Univ British Columbia, Dept Psychiat, Townsend Family Labs, Vancouver, BC, Canada

[5] Univ Ghent, Dept Basic Med Sci, Physiol Grp, Ghent, Belgium

[6] Univ British Columbia, Inst Life Sci, Dept Cellular & Physiol Sci, Vancouver, BC, Canada

来源：

NEUROSCIENCE LETTERS | 2019年 / 695卷

关键词：

Gap junctions; Connexin; Pannexin; Alzheimer's; Hemichannel; ENDOTHELIAL CALCIUM DYNAMICS; FUNCTIONAL GAP-JUNCTIONS; A-BETA-PLAQUES; MAST-CELLS; ENDOPLASMIC-RETICULUM; AMYLOID PLAQUES; MIMETIC PEPTIDE; CLEAVAGE SITE; ATP RELEASE; GLIAL-CELLS;

D O I：

10.1016/j.neulet.2017.09.006

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

By 2040 neurodegenerative diseases will become the world's second leading cause of death after cardiovascular disease (WHO). Major efforts are required to elucidate the underlying molecular and cellular mechanisms of neurodegenerative diseases. Connexin and pannexin membrane channel proteins are conduits through which neuronal, glial, and vascular tissues interact. In the normal brain, this interaction underlies homeostasis, metabolic supply and neuroprotection. In models of neuroinflammation these channels present aberrant functioning. Validation of the molecular mechanisms by which these membrane channels influence neurodegeneration particularly in Alzheimer's disease could lead to new and alternative therapeutic strategies targeting these channels.

引用

页码：100 / 105

页数：6

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