Synaptic roles of cyclin-dependent kinase 5 & its implications in epilepsy

被引:16
|
作者
Dixit, Aparna Banerjee [1 ]
Banerjee, Jyotirmoy [1 ]
Tripathi, Manjari [2 ]
Sarkar, Chitra [3 ]
Chandra, P. Sarat [4 ]
机构
[1] All India Inst Med Sci AIIMS Collaborat, NBRC, Ctr Excellence Epilepsy, Gurugram 122051, Haryana, India
[2] AIIMS, Dept Neurol, New Delhi, India
[3] AIIMS, Dept Pathol, New Delhi, India
[4] AIIMS, Dept Neurosurg, New Delhi, India
关键词
Cyclin-dependent kinase 5; epilepsy; epileptogenesis; neurodegenerative diseases; pharmacoresistant; seizures; synaptic plasticity; ACTIVATED PROTEIN-KINASE; CDK5; PHOSPHORYLATES; DNA-DAMAGE; P35; HIPPOCAMPAL; LOCALIZATION; EXPRESSION; AMPHIPHYSIN-1; ORGANIZATION; PLASTICITY;
D O I
10.4103/ijmr.IJMR_1249_14
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
There is an urgent need to understand the molecular mechanisms underlying epilepsy to find novel prognostic/diagnostic biomarkers to prevent epilepsy patients at risk. Cyclin-dependent kinase 5 (CDK5) is involved in multiple neuronal functions and plays a crucial role in maintaining homeostatic synaptic plasticity by regulating intracellular signalling cascades at synapses. CDK5 deregulation is shown to be associated with various neurodegenerative diseases such as Alzheimer's disease. The association between chronic loss of CDK5 and seizures has been reported in animal models of epilepsy. Genetic expression of CDK5 at transcriptome level has been shown to be abnormal in intractable epilepsy. In this review various possible mechanisms by which deregulated CDK5 may alter synaptic transmission and possibly lead to epileptogenesis have been discussed. Further, CDK5 has been proposed as a potential biomarker as well as a pharmacological target for developing treatments for epilepsy.
引用
收藏
页码:178 / 187
页数:10
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