The role of calpain in spinal cord degeneration in experimental Pаrkinson’s disease

Abstract

In this review the critical role of Са2+-dependent protease calpain in the cascade of intracellular processes, leading to degeneration and death of spinal cord neurons in experimental models of Parkinson’s disease (PD) is discussed. In experimental conditions parkinsonian neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone cause the activation of calpain and caspase-3, which subsequently cleave cytoskeletal protein spectrin and axonal neurofilament light protein (NF-L). In the absence of the protease inhibitors, these processes can lead to structural and functional alterations in neurons and axons. It has been demonstrated that calpain inhibition provides neuroprotection in the spinal cord in experimental PD.