Genes Teach Us About Parkinson's Disease, Part 2
In my last post I was describing how, according to TheScientist
(2/1/11), genetic forms of Parkinson’s Disease can teach medical researchers possible causes for non-genetic forms.
In certain genetic cases, a gene involved in releasing neurotransmitters is mutated so that it makes too much product. When this happens, the excess product seems to result in fibrous bundles found in the brains of Parkinson’s sufferers. But even with the normal gene, over-production can occur. And such over-production seems to be connected to problems with mitochondria, the cell organelles that produce energy molecules from food. So dysfunctional mitochondria may be associated with Parkinson’s disease. Possible treatments might need to start with mitochondria.
In certain other genetic cases, genes are mutated so that they produce to little or no product. Interestingly, these genes also have to do with mitochondrial function. Again, these genes point to possible treatments.
To me, what is really intriguing about all this, aside from the possible paths to alleviation of the disease, is the connection with energy pathways in the neurons involved in Parkinson’s Disease. When researchers finally are able to clarify the “mitochondrial connection,” what will they find? Exactly how does energy production change dopamine production? What else might be involved? It will be fascinating to find out