Abstract

Alzheimer’s disease (AD) is a neurodegenerative confusion associated with dementia. AD is indicated by progressive loss of memory. It is having characteristic evidence of β-amyloid extracellularly and neurofibrillary tangle’s development intracellularly. Neurons lose the capability of cell division after they attain full development. Cyclin dependent kinase 5 (Cdk5) is a kinase protein which is neuron specific and plays a vital role in the movement of newly developed neurons. When Cdk5 is dysregulated, then several diseases like AD, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) may occur. The Cdk5 phosphorylation takes place as a result of change of N-methyl-D-aspartate (NMDA) receptor activity and expression, neurotransmitter release, degradation of synaptic proteins, or in-gene expression modulation, which leads to the activation of Cdk5. The activated calpain proteins convert p35 activator of Cdk5 into p25, which causes remarkable  activation  of the Cdk5. This highly  activates Cdk5-p25 complex hyperphosphorylates, the Tau protein, which causes the release of microtubules and gathers as cytoplasmic filaments. This leads to  tangle formation that leads to neuronal cell death. In AD brain, the Cdk5 is present in a highly activated form. This review article emphasizes the role of cyclin dependent kinase 5 in AD.   Key words: Alzheimer’s disease, β-amyloid plaques, CDK5, neurodegeneration, neurofibrillary tangle.

Highlights

  • Alzheimer’s disease (AD) is one of the main causes of dementia

  • AD was originally defined as presenile dementia, but it appears that the same pathology underlies the dementia irrespective of the age of onset (Rang and Dale, 2007)

  • It is concluded that the Cyclin dependent kinase 5 (Cdk5) plays a vital role in the brain development through its involvement in the processes of neuronal migration

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Summary

INTRODUCTION

AD is one of the main causes of dementia. The occurrence of AD increases with age (James et al, 2008; Kang et al, 1987). AD is characterized by the progressive loss of memory related to the decline in language, visuospatial function, estimation and decision. It leads to major behavioral and functional disability (James et al, 2008; Chung, 2009). The role of cdk in guiding new neurons to their proper place has been discovered, which has increased the understanding of adult neurogenesis, improved understanding of its involvement in cognitive function and brightened the expectations for brain cell therapy (Albert et al, 2009). The localization of fibrous insoluble proteins inside the brain is a characteristic features of several disorders, including AD, PD and Lewy body dementia (LBD) (Mierczak et al, 2011)

PATHOGENESIS OF AD
NEURONAL CELL CYCLE IN PATHOGENESIS OF AD
THE CDK FAMILY
LOSS OF NEURONAL CELL CYCLE CONTROL IN AD
THE NEUROGENESIS PROCESS
Findings
CONCLUSION

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