October Update

Bought a standard poodle puppy.  Bringing him home October 5, so October will be full of housebreaking, and FUN.



Entries in Parkinson's Disease (2)


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 


Genes Teach Us About Parkinson's Disease, Part 1

Parkinson’s Disease occurs when the brain cells that produce the neurotransmitter dopamine deteriorate.  The result may be shaking and difficulty with walking, movment, and coordination.  There is no cure.

         It’s sad but true that we learn more in biology when things go wrong than when things go right.  If a process is going along normally, we can’t see the parts of that process.  But if one or a few parts of the malfunction, suddenly the gaps highlight the missing steps, and we understand the normal process better.

         This has happened with the discovery of genes associated with Parkinson’s Disease.  Even though only a small percentage of cases of Parkinson’s Disease are caused or exacerbated by gene malfunctions, those genes are enlightening Parkinson’s researchers.

         Interestingly, a lot of the genes in question have to do with oxidation and/or waste clean-up in dopamine producing brain cells.  Ultimately this information could lead to new treatments for the disease.  

         If too much of a gene product is gumming up neurons, it could be that stopping or slowing that gene product could prevent the damage.  And it could be that even if the gene is normal in some Parkinson’s sufferers, an environmental factor is causing the same problem.  In that case, the cure might be similar.

         Alternatively, too little of a different gene product might interfere with normal cell clean-up.  The resulting waste accumulation could also gum things up.  Again, environmental factors could mimic this problem.  In either case, some way of supplying the missing molecule(s) might help.

         Food for thought.  I’ll say more about this in my next post.