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Scientists have discovered a process by which the "power plants" of the brain - tiny mitochondria found inside cells - signal that they are damaged and need to be eliminated. This is according to a study published in the journal Nature Cell Biology.
Previous research has provided evidence that many neurological disorders may be caused by impaired mitochondrial function.
Last year, Medical News Today reported on a study that suggested mitochondrial impairment may lead to mood and psychotic disorders.
Now, researchers from the University of Pittsburgh say their findings have opened the door to potential research into cures for diseases that are believed to be caused by dysfunctional mitochondria in neurons, such as Parkinson's disease.
The researchers explain that mitochondria contain a component on their inner membranes called cardiolipins. When a mitochondrion is damaged, the cardiolipins move from the inner membrane to the outer membrane, encouraging the cell to destroy the entire mitchondrion.
Dr. Valerian Kagan, professor and vice chair of the Department of the Environmental and Occupational Health at the Pitt Graduate School of Public Health, says the process is similar to cooking a Thanksgiving turkey:
"You put the turkey in the oven and the outside becomes golden, but you can't just look at it to know it's ready. So you put a thermometer in, and when it pops up, you know you can eat it," he explains.
"Mitochondria give out a similar 'eat me' signal to cells when they are done functioning properly."
The next stage of the process involves a protein called LC3. One part of this protein binds to cardiolipin, causing a "specialized structure" to form around the mitochondrion which carries it to the digestive centers of the cell.
Dr. Kagan explains:
"It's a survival process. Cells activate to get rid of bad mitochondria and consolidate good mitochondria. If this process succeeds, then the good ones can proliferate and the cells thrive.
It's a beautiful, efficient mechanism that we will seek to target and model in developing new drugs and treatments."
Dr. Hülya Bayir, research director of pediatric clinical care medicine at the Children's Hospital of Pittsburgh, explains that although this process happens in all cells with mitochondria, it is very important that it functions correctly in neuronal cells "because these cells do not divide and regenerate as readily as cells in other pats of the body."
"I think these findings have huge implications for brain injury patients. The mitochondrial 'eat me' signaling process could be a therapeutic target in the sense that you need a certain level of clearance of damaged mitochondria," she adds.
"But, on the other hand, you don't want the clearing process to go on unchecked. You must have a level of balance, which is something we could seek to achieve with medications or therapy if the body is not able to find that balance itself."
The study authors say that further research is to be conducted in order to determine exactly what prompts the cardiolipin to move outside the mitochondria, and how this fits with other pathways that affect the development of Parkinson's disease.
They note that two relating Parkinson's disease genes are also linked to the removal of mitochondria.
Medical News Today recently reported on a study that suggested a chemical used in anti-wrinkle cream may prevent early-onset Parkinson's disease.
Written by Honor Whiteman
Copyright: Medical News Today
Not to be reproduced without the permission of Medical News Today.
Cardiolipin externalization to the outer mitochondrial membrane acts as an elimination signal for mitophagy in neuronal cells, doi:10.1038/ncb2837, published online in Nature Cell Biology, 15 September 2013. Abstract
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