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Neurodegenerative protein role revealed as drug target

By Wai Lang Chu , 07-Jun-2006

New research has suggested that that pharmacological inhibition of a protein's role in Alzheimer's, Parkinson's and cancer research could be key to either preventing or promoting cell death.

Two studies performed by Canadian researchers demonstrated that the protein calpain promoted programmed cell death after chemicals that disrupt the endoplasmic reticulum - a major synthetic structure in the cell that controls the synthesis and distribution of new proteins - damaged cells.

"The work provides proof that drug treatment of calpain may be used to block cell death in situations where this is not desirable, such as in neuronal cells of Alzheimer's or Parkinson's patients, but to promote cell death in cancer cells where this is clearly a very desirable outcome," said lead researcher Peter Greer.

Cells in the body have the ability to trigger an intrinsic programmed cell death response.

"In the case of nerve cells that have been temporarily cut off from their oxygen supply because of a stroke, or damaged by amyloid deposits, this might seem like a bad thing that could contribute to neurodegenerative disease," added Greer.

"On the other hand, when a cell's chromosomes are damaged by carcinogens or ultraviolet light in a way that could initiate cancer, this same programmed cell death response could save your life."

In the second study, both published in >JBC online , investigators found that calpain also inhibited programmed cell death in response to other challenges, including some chemotherapeutic drugs.

This study also showed that calpain contributes to the activation of AKT and JNK, two key players in the signalling pathways that control cellular responses to different death stimuli.

These discoveries suggest that calpain inhibitors might improve the ability of chemotherapeutic drugs or radiation treatment to specifically kill tumour cells in cancer patients.

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