阿尔茨海默病中的钙紊乱机制研究进展

被引:8
作者
陈艳杏
孙圣刚
机构
[1] 华中科技大学同济医学院附属协和医院神经内科
关键词
阿尔茨海默病; 钙; 钙紊乱; 钙稳态;
D O I
10.16636/j.cnki.jinn.2009.05.019
中图分类号
R749.16 [];
学科分类号
100203 ;
摘要
阿尔茨海默病是最常见的神经变性病,也是老年痴呆最常见的形式,其发病机制已得到广泛而深入的研究,并为临床药物治疗提供了理论基础。阿尔茨海默病中的钙紊乱机制很早就已经提出,并被后来的研究不断论证和补充。近年来对钙调节机制在阿尔茨海默病发病中的作用研究又取得了很大的进展,包括家族性痴呆变异基因引起的钙紊乱机制的研究,新的基因多态性的发现等,这些研究结果为进一步了解阿尔茨海默病的发病机制提供了新的视点,将为临床药物治疗提供新的靶点。
引用
收藏
页码:441 / 444
页数:4
相关论文
共 11 条
[1]   阿尔茨海默病中β淀粉样蛋白与内质网应激的相关研究 [J].
罗红波 ;
杨期东 .
国际神经病学神经外科学杂志, 2007, (06) :524-527
[2]  
A Polymorphism in CALHM1 Influences Ca 2+ Homeostasis, Aβ Levels, and Alzheimer's Disease Risk[J] . Ute Dreses-Werringloer,Jean-Charles Lambert,Valérie Vingtdeux,Haitian Zhao,Horia Vais,Adam Siebert,Ankit Jain,Jeremy Koppel,Anne Rovelet-Lecrux,Didier Hannequin,Florence Pasquier,Daniela Galimberti,Elio Scarpini,David Mann,Corinne Lendon,Dominique Campion,Philippe Amouyel,Peter Davies,J. Kevin Foskett,Fabien Campagne,Philippe Marambaud.Cell . 2008 (7)
[3]   Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating [J].
Cheung, King-Ho ;
Shineman, Diana ;
Mueller, Marioly ;
Cardenas, Cesar ;
Mei, Lijuan ;
Yang, Jun ;
Tomita, Taisuke ;
Iwatsubo, Takeshi ;
Lee, Virginia M. -Y. ;
Foskett, J. Kevin .
NEURON, 2008, 58 (06) :871-883
[4]   Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks [J].
Kuchibhotla, Kishore V. ;
Goldman, Samuel T. ;
Lattarulo, Carli R. ;
Wu, Hai-Yan ;
Hyman, Bradley T. ;
Bacskai, Brian J. .
NEURON, 2008, 59 (02) :214-225
[5]   Pore-forming proteins share structural and functional homology with amyloid oligomers [J].
Yoshiike, Yuji ;
Kayed, Rakez ;
Milton, Saskia C. ;
Takashima, Akihiko ;
Glabe, Charles G. .
NEUROMOLECULAR MEDICINE, 2007, 9 (03) :270-275
[6]   Calcium buffering systems and calcium signaling in aged rat basal forebrain neurons [J].
Murchison, David ;
Griffith, William H. .
AGING CELL, 2007, 6 (03) :297-305
[7]  
Presenilins Form ER Ca 2+ Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations[J] . Huiping Tu,Omar Nelson,Arseny Bezprozvanny,Zhengnan Wang,Sheu-Fen Lee,Yi-Heng Hao,Lutgarde Serneels,Bart De Strooper,Gang Yu,Ilya Bezprozvanny.Cell . 2006 (5)
[8]   Ca2+ regulation and gene expression in normal brain aging [J].
Toescu, EC ;
Verkhratsky, A ;
Landfield, PW .
TRENDS IN NEUROSCIENCES, 2004, 27 (10) :614-620
[9]   Annexin 5 and apolipoprotein E2 protect against Alzheimer's amyloid-β-peptide cytotoxicity by competitive inhibition at a common phosphatidylserine interaction site [J].
Lee, G ;
Pollard, HB ;
Arispe, N .
PEPTIDES, 2002, 23 (07) :1249-1263
[10]  
Subfield- and layer-specific changes in parvalbumin, calretinin and calbindin-D28k immunoreactivity in the entorhinal cortex in Alzheimer's disease[J] . M. Mikkonen,I. Alafuzoff,T. Tapiola,H. Soininen,R. Miettinen.Neuroscience . 1999 (2)