Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1792, Issue 8, Pages 741-745Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2009.05.001
Keywords
Cyclin-dependent kinase 5 (Cdk5); Synapse; NMDA receptor; Dendritic spine; Transcription factor; Learning and memory
Funding
- Research Grants Council of Hong Kong [6119/04M, 6421/05M, 6431/06M, 6444/06M, 1/06C]
- University Grants Committee [AoE/B-15/013]
- Hong Kong Jockey Club
- Croucher Foundation Senior Research Fellow
- Croucher Foundation Fellow
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The molecular composition of the postsynaptic density is modified during synaptic plasticity, which forms the molecular basis of learning and memory. Such changes in synaptic composition depends in part on the intricate regulation of phosphorylation of specific proteins via different protein kinases, including a serine/threonine kinase, cyclin-dependent kinase 5 (Cdk5). However, the mechanisms underlying the involvement of Cdk5 in neural plasticity remain elusive. Recently, the identification of a number of synaptic proteins as substrates or interacting proteins with Cdk5 provides important clues on how this kinase modulates the efficacy of synaptic transmission. In this review, we summarize the recent findings to illustrate the multifaceted roles of Cdk5 in synaptic plasticity through affecting dendritic spine formation, ion channel conductance, protein expression, and transcription in the postsynaptic neurons. Importantly, dysregulation of Cdk5 has been linked to Alzheimer's disease, which involves perturbations in synaptic functions and memory formation. Understanding the mechanisms by which Cdk5 regulates synaptic plasticity may therefore provide important insights in the design of novel therapeutic strategies for neurodegenerative diseases. (C) 2009 Elsevier B.V. All rights reserved.
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