New developments on the role of NMDA receptors in Alzheimer's disease

被引：105
作者：
Malinow, Roberto [1 ,2 ]
机构：
[1] Univ Calif San Diego, Dept Neurosci, Ctr Neural Circuits & Behav, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Ctr Neural Circuits & Behav, Div Biol, La Jolla, CA 92093 USA
来源：
CURRENT OPINION IN NEUROBIOLOGY | 2012年 / 22卷 / 03期
关键词：
AMYLOID PRECURSOR PROTEIN; LONG-TERM POTENTIATION; DENDRITIC SPINE LOSS; IN-VIVO; BETA PROTEIN; SYNAPTIC PLASTICITY; MOUSE MODELS; SIGNALING PATHWAY; TRANSGENIC MICE; OLIGOMERS;
D O I：
10.1016/j.conb.2011.09.001
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Since the initial findings that NMDA receptors play important roles in cellular models of learning as well as neurotoxicity, abnormal function of this receptor has been considered a potential mechanism in the pathophysiology underlying Alzheimer's disease. Treatment of Alzheimer's disease with an NMDA receptor antagonist began several years ago, with some limited success. More recent mechanistic studies have examined the role of NMDA receptors in the synaptic effects of beta amyloid (A beta).
引用
收藏
页码：559 / 563
页数：5
相关论文
共 52 条
[1]   Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses [J].
Almeida, CG ;
Tampellini, D ;
Takahashi, RH ;
Greengard, P ;
Lin, MT ;
Snyder, EM ;
Gouras, GK .
NEUROBIOLOGY OF DISEASE, 2005, 20 (02) :187-198
[2]   Subunit-specific NMDA receptor trafficking to synapses [J].
Barria, A ;
Malinow, R .
NEURON, 2002, 35 (02) :345-353
[3]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[4]   Activation of Extrasynaptic, But Not Synaptic, NMDA Receptors Modifies Amyloid Precursor Protein Expression Pattern and Increases Amyloid-β Production [J].
Bordji, Karim ;
Becerril-Ortega, Javier ;
Nicole, Olivier ;
Buisson, Alain .
JOURNAL OF NEUROSCIENCE, 2010, 30 (47) :15927-15942
[5]   Clusters of hyperactive neurons near amyloid plaques in a mouse model of Alzheimer's disease [J].
Busche, Marc Aurel ;
Eichhoff, Gerhard ;
Adelsberger, Helmuth ;
Abramowski, Dorothee ;
Wiederhold, Karl-Heinz ;
Haass, Christian ;
Staufenbiel, Matthias ;
Konnerth, Arthur ;
Garaschuk, Olga .
SCIENCE, 2008, 321 (5896) :1686-1689
[6]   Rapid, concurrent alterations in pre- and postsynaptic structure induced by naturally-secreted amyloid-β protein [J].
Calabrese, Barbara ;
Shaked, Gideon M. ;
Tabarean, Iustin V. ;
Braga, Julia ;
Koo, Edward H. ;
Halpain, Shelley .
MOLECULAR AND CELLULAR NEUROSCIENCE, 2007, 35 (02) :183-193
[7]   Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice [J].
Chapman, PF ;
White, GL ;
Jones, MW ;
Cooper-Blacketer, D ;
Marshall, VJ ;
Irizarry, M ;
Younkin, L ;
Good, MA ;
Bliss, TVP ;
Hyman, BT ;
Younkin, SG ;
Hsiao, KK .
NATURE NEUROSCIENCE, 1999, 2 (03) :271-276
[8]   Alzheimer amyloid β-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus [J].
Chen, QS ;
Wei, WZ ;
Shimahara, T ;
Xie, CW .
NEUROBIOLOGY OF LEARNING AND MEMORY, 2002, 77 (03) :354-371
[9]   Synaptic activity regulates interstitial fluid amyloid-β levels in vivo [J].
Cirrito, JR ;
Yamada, KA ;
Finn, MB ;
Sloviter, RS ;
Bales, KR ;
May, PC ;
Schoepp, DD ;
Paul, SM ;
Mennerick, S ;
Holtzman, DM .
NEURON, 2005, 48 (06) :913-922
[10]   Reversing EphB2 depletion rescues cognitive functions in Alzheimer model [J].
Cisse, Moustapha ;
Halabisky, Brian ;
Harris, Julie ;
Devidze, Nino ;
Dubal, Dena B. ;
Sun, Binggui ;
Orr, Anna ;
Lotz, Gregor ;
Kim, Daniel H. ;
Hamto, Patricia ;
Ho, Kaitlyn ;
Yu, Gui-Qiu ;
Mucke, Lennart .
NATURE, 2011, 469 (7328) :47-52
123456