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.

Abbreviation

AD, Alzheimer’s disease; NFTs, neurofibrillary tangles; sAPP, secreted amyloid precursor protein; HD, Huntington’s disease; ALS, amyotrophic lateral sclerosis.