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Dr. Robert Korneluk from the University of Ottawa, Canada, and his team have been able to show that the inhibition of an intricate control system to balance cell proliferation and cell death, called apoptosis or programmed cell death, can rescue the function of neurons in the central nervous system.
At the international conference "Neurodegenerative Diseases: Molecular Mechanisms in a Functional Genomics Framework" in the Max Delbrück Communications Center (MDC.C) Berlin, Germany, Dr. Korneluk reported that this was shown in animal models for human neurodegenerative disorders such as retinal eye disease and Parkinson's disease.
In a wide variety of neurodegenerative diseases the nerve cells progressively die leading to severe motor dysfunction, mental decline and eventually death.
Apoptosis is a safety system in cells, which enables damaged cells to literally commit suicide to protect the organism as a whole.
This programme appears to be a primary defect in cancer cells. Cancer researchers therefore aim to activate this programme for cancer therapy, inducing apoptosis in tumour cells that have lost this function and, therefore, continue to grow indefinitely.
Ten years ago, Dr. Korneluk, Professor of Paediatrics, and researchers from the Apoptosis Research Centre at the Children`s Hospital of Eastern Ontario Research Institute in Ottawa, discovered a family of genes that control apoptosis.
"These Inhibitors Apoptosis (IAP) genes are highly conserved from insects to humans. Their proteins are potent suppressors of programmed cell death", he said in Berlin.
"They directly bind and inhibit caspases, enzymes that are key executioners of cell death and thus play a critical role in deciding cell fate. The IAPs are the only known intrinsic inhibitors of caspases, that are central to both the initiation and the execution of the apoptotic cascade."
"Increasing the expression of IAP genes has been shown to protect cells from apoptosis induction", Dr. Korneluk said. For example we have demonstrated that a gene therapy approach to increase IAP activity is protective in animal models of Parkinson's disease, Retinitis Pigmentosa (RP, an inherited retinal eye disease) and stroke.
Therefore, strategies to increase the level of IAP expression in neurons, that are compromised by a neurodegenerative condition, should be effective in the treatment of these disorders.
The four-day conference, which started on September 6, is organized by the Max Delbrück Center for Molecular Medicine (MDC), the Charité Universitätsmedizin Berlin, and the University of Bonn (all in Germany). 200 clinicians and researchers from Canada, Europe, Japan, and the USA discuss their latest findings there.
Press and Public Affairs
Max Delbrück Center for Molecular Medicine(MDC) Berlin-Buch
Barbara Bachtler
Robert-Rössle-Str. 10
13125 Berlin, Germany
Phone: +49/30/9406-38 96
Fax.: +49/30/9406-38 33
e-mail: bachtler@mdc-berlin.de
http://www.mdc-berlin.de/englisch/about_the_mdc/public_relations/e_index.htm
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