Abstract

Fasna V*, Bijesh vatakkeel, R. Raji and Adhya Das

ABSTRACT

Cyclin-dependent kinase 5 (Cdk5) is a member of a family of proline-directed serine/threonine kinase. Cdk5 plays a critical role in the development of the nervous system, including neuronal migration and differentiation. Unlike the other Cdk family members, Cdk5 is neither directly engaged in cell cycle regulation nor is it controlled by cyclins. Dopaminergic signalling, release of neurotransmitters, membrane cycling and other synaptic functions are all impacted by Cdk5. The two Cdk5 activators are p35 and p39, which control the spatial and temporal expression of active Cdk5 in order to limit its activity largely to post-mitotic neurons. Despite playing a crucial part in central nervous system development, dysregulation of Cdk5 has been linked to a number of diseases including Alzheimer's disease, Amyotrophic lateral sclerosis, Parkinson's disease etc. When Cdk5 is associated with p25, a shortened version of the typical activator p35, it becomes overactivated and relocalizes in these neurodegenerative diseases, ultimately resulting in neuronal death. It is important to note that Cdk5 inhibitors have been demonstrated to have neuroprotective benefits by preventing associated degenerative processes. With a focus on current developments in Cdk5 in neurological illnesses and the possibility of targeting Cdk5 for the treatment of neurological disorders, this review will briefly describe the physiological and pathological mechanisms of Cdk5 in the nervous system.