GluN2B-NMDA receptors in Alzheimer's disease:beyond synapse loss and cell death  被引量:1

GluN2B-NMDA receptors in Alzheimer's disease:beyond synapse loss and cell death

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作  者:Qiang Zhou 

机构地区:[1]School of Chemical Biology and Biotechnology Peking University Shenzhen Graduate School

出  处:《Neural Regeneration Research》2014年第21期1878-1879,共2页中国神经再生研究(英文版)

摘  要:Alzheimer's disease (AD) is one of the most devastating dis- eases affecting the life and health of aging population. Two hallmarks of AD are senile plaques and neurofibrillary tan- gles, and AD is well known for the massive loss of neurons and impaired cognitive functions especially memory loss. Despite extensive search for effective treatment, available drugs have limited efficacy without affecting the course of AD. Significant efforts have been devoted to curb the pro- duction of amyloid [3 (A[3; the major component of plaques) or enhance the clearance of it, with the aim to reduce the accumulation of plaque in the brain. Antibodies that can bind A[3 to increase their removal have received a lot of at- tention although recent clinical trial results have been largely negative and disappointing (Panza et al., 2014). Targets that are not directly related to A[3 have also been pursued. One such target is N-methyl-D-aspartate (NMDA) receptors (NMDARs), a subclass of glutamate receptors. The antago- nist of NMDAR memantine has been approved for treating moderate to severe AD, although the exact mechanism un- derlying its action is still in debate (Kotermanski and John- son, 2009).Alzheimer's disease (AD) is one of the most devastating dis- eases affecting the life and health of aging population. Two hallmarks of AD are senile plaques and neurofibrillary tan- gles, and AD is well known for the massive loss of neurons and impaired cognitive functions especially memory loss. Despite extensive search for effective treatment, available drugs have limited efficacy without affecting the course of AD. Significant efforts have been devoted to curb the pro- duction of amyloid [3 (A[3; the major component of plaques) or enhance the clearance of it, with the aim to reduce the accumulation of plaque in the brain. Antibodies that can bind A[3 to increase their removal have received a lot of at- tention although recent clinical trial results have been largely negative and disappointing (Panza et al., 2014). Targets that are not directly related to A[3 have also been pursued. One such target is N-methyl-D-aspartate (NMDA) receptors (NMDARs), a subclass of glutamate receptors. The antago- nist of NMDAR memantine has been approved for treating moderate to severe AD, although the exact mechanism un- derlying its action is still in debate (Kotermanski and John- son, 2009).

关 键 词:GluN2B-NMDA receptors in Alzheimer’s disease NMDA NMDAR 

分 类 号:R749.16[医药卫生—神经病学与精神病学]

 

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