Copper as a Collaborative Partner of Zinc-Induced Neurotoxicity in the Pathogenesis of Vascular Dementia

被引:13
|
作者
Kawahara, Masahiro [1 ]
Tanaka, Ken-ichiro [1 ]
Kato-Negishi, Midori [1 ]
机构
[1] Musashino Univ, Res Inst Pharmaceut Sci, Fac Pharm, Dept Bioanalyt Chem, Tokyo 2028585, Japan
关键词
zinc; endoplasmic reticulum; MAP kinase; calcium homeostasis; mitochondria; synapse; AMYLOID PRECURSOR PROTEIN; NEURONAL DEATH; CORTICAL-NEURONS; PRION PROTEIN; GNRH NEURONS; CA2+ CHANNEL; CELL-DEATH; ZN2+; CARNOSINE; STRESS;
D O I
10.3390/ijms22147242
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Copper is an essential trace element and possesses critical roles in various brain functions. A considerable amount of copper accumulates in the synapse and is secreted in neuronal firings in a manner similar to zinc. Synaptic copper and zinc modulate neuronal transmission and contribute to information processing. It has been established that excess zinc secreted during transient global ischemia plays central roles in ischemia-induced neuronal death and the pathogenesis of vascular dementia. We found that a low concentration of copper exacerbates zinc-induced neurotoxicity, and we have demonstrated the involvement of the endoplasmic reticulum (ER) stress pathway, the stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) signaling pathway, and copper-induced reactive oxygen species (ROS) production. On the basis of our results and other studies, we discuss the collaborative roles of copper in zinc-induced neurotoxicity in the synapse and the contribution of copper to the pathogenesis of vascular dementia.
引用
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页数:14
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