淀粉样β-蛋白在阿尔茨海默病突触可塑性中的作用

被引:11
作者
张锦辉
郑琳琳
机构
[1] 辽东学院医学院
关键词
阿尔茨海默病; 淀粉样β-蛋白; 突触可塑性;
D O I
10.14168/j.issn.1673-4939.2014.02.010
中图分类号
R749.16 [];
学科分类号
摘要
阿尔茨海默病是老年痴呆的常见类型,与年龄密切相关,目前AD的确切发病机制仍不十分清楚。AD发生后脑内出现老年斑,其核心成分为淀粉样β-蛋白(amyloidβ-peptide,Aβ)。Aβ在脑内的异常沉积导致突触可塑性降低,影响海马长时程增强过程。研究表明Aβ发挥神经毒性作用主要是其寡聚体,如Aβ1-40和Aβ1-42等,使N-甲基-D-天冬氨酸(NMDA)的受体失活,导致NMDA受体介导的谷氨酸异常增高,最终体现为学习记忆能力下降。
引用
收藏
页码:95 / 98
页数:4
相关论文
共 8 条
[1]
Apolipoprotein E4 effects in Alzheimer’s disease are mediated by synaptotoxic oligomeric amyloid-β.[J].Robert M. Koffie;Tadafumi Hashimoto;Hwan-Ching Tai;Kevin R. Kay;Alberto Serrano-Pozo;Daniel Joyner;Steven Hou;Katherine J. Kopeikina;Matthew P. Frosch;Virginia M. Lee;David M. Holtzman;Bradley T. Hyman;Tara L. Spires-Jones.Brain.2012, 7
[2]
Selective presynaptic degeneration in the synaptopathy associated with ME7-induced hippocampal pathology [J].
Gray, Bryony C. ;
Siskova, Zuzana ;
Perry, V. Hugh ;
O'Connor, Vincent .
NEUROBIOLOGY OF DISEASE, 2009, 35 (01) :63-74
[3]
Controlled in situ preparation of Aβ(1–42) oligomers from the isopeptide “iso-Aβ(1–42)”; physicochemical and biological characterization.[J]..Peptides.2009, 2
[4]
Mixed brain pathologies account for most dementia cases in community-dwelling older persons [J].
Schneider, Julie A. ;
Arvanitakis, Zoe ;
Bang, Woojeong ;
Bennett, David A. .
NEUROLOGY, 2007, 69 (24) :2197-2204
[5]
The levels of soluble versus insoluble brain Aβ distinguish Alzheimer's disease from normal and pathologic aging [J].
Wang, J ;
Dickson, DW ;
Trojanowski, JQ ;
Lee, VMY .
EXPERIMENTAL NEUROLOGY, 1999, 158 (02) :328-337
[6]
Soluble amyloid β peptide concentration as a predictor of synaptic change in Alzheimer's disease [J].
Lue, LF ;
Kuo, YM ;
Roher, AE ;
Brachova, L ;
Shen, Y ;
Sue, L ;
Beach, T ;
Kurth, JH ;
Rydel, RE ;
Rogers, J .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (03) :853-862
[7]
Block of LTP in rat hippocampus in vivo by β-amyloid precursor protein fragments.[J].William K. Cullen;Yoo-Hun Suh;Roger Anwyl;Michael J. Rowan.NeuroReport.1997, 15
[8]
Reversion of β 25–35 -amyloid peptide-induced amnesia by NMDA receptor-associated glycine site agonists.[J].Tangui Maurice;Brian P. Lockhart;Tsung-Ping Su;Alain Privat.Brain Research.1996, 1