Protein Link Between Parkinson’s and Alzheimer’s

I think it is safe to say that everyone knows what Protein is at least in terms of food and nutrition, but not everyone might realize how much different protein molecules play vital roles in our bodies and in our brains.

First, exactly what is a protein at the molecular level? A fairly simple definition is that proteins are strings of amino acids that our bodies get from food and/or make themselves. These “strings” can then “fold” in several different ways and also interact with other proteins. A reasonable visual representation would be to think of them as a string of beads (amino acids) that is folded around itself and interwoven with other strings of beads. Obviously this is a fairly simplified example, but I think it gets the picture across.

Now, what does this have to do with Parkinson’s Disease or Alzheimer’s Disease? Well, proteins play many roles in our bodies, from forming muscles to helping neurons to communicate in our brains. In PD a particular protein, a-synuclein, is proposed to play a critical role in the formation of Lewy Bodies, a tell-tale sign of PD. Lewy Bodies are essentially the accumulation of a bunch of a-synuclein proteins and are known to cause disruption to neurons. In Alzheimer’s the Abeta amyloid protein is implicated in the formation of plaques which in turn cause the neurological difficulties experienced by Alzheimer’s patients. It is known clinically that a person who develops either PD or Alzheimer's is at a significantly higher risk to develop the other disease.

A new study conducted at the University of California at San Diego used super computers to help analyze how these two specific proteins interact and to explore why people with either Alzheimer’s or Parkinson’s disease have a higher risk for also developing the other neurological disorder. The researchers discovered that abnormal interactions between a-synuclein and Abeta amyloid can lead to the creation of “hybrid” complexes which result in a combination of Alzheimer’s and Parkinson’s. Using the computer models researchers were able to see the new hybrid protein form with a small hole called a “nanopore”. This hybrid disrupts neuronal activity.

The interesting part of this finding to me is that researchers have now shown at least one clear path of how Parkinson’s and Alzheimer’s are related in a molecular way. To me this finding clearly shows how solving the puzzle of one disease will have a dramatic impact on the other. If such a clear connection can be shown in these two diseases what other connections are there to other neurological disorders like ALS, MS, Huntington’s Disease, etc? How do we unlock the mystery of any of these diseases so that we can then solve all of the others? I am still convinced that curing or preventing one of these many diseases will be the key to curing them all.

As always here is the link to the study.
http://www.sciencedaily.com/releases/2008/09/080903204225.htm

New Finding with Deep Brain Stimilation

Could Deep Brain Stimulation(DBS) Stop the Progression of Parkinson's Disease???? Researchers at the University of Cincinnati and University Hospital are saying "Yes". A new study conducted by Caryl Sortwell, PhD and Michael Behbehani, PhD suggests that with a certain percentage of DBS patients that is the case. The study indicates that a protein in the brain called BDNF (brain-derived neurotrophic factor) is increased by the technique. This protein is known to be a tropic factor that provides "a nurturing, growth chemical" and it is thought that it may be responsible for the slow down in progression that some patients exist.

The study does note that not all patients seem to have the same results from DBS. Some patients have a marked decrease in symptoms and a slower progression while others do not. There is no discussion of why some patients respond so positively while others do not.

I personally hope that more research will be done to isolate the difference among different patients to help find a way to help all patients. I would also love to see if there are other ways to increase BDNF in the brains of PD patients using other techiques. Could it be possible that this particular protein could help increase the quality of life for PD patients for numerous years? Could the brain help repair itself if the neuronal death is slowed or stopped? I am of the opinion that further research into these areas and questions is needed and needed soon.

To read one article about this study please click the link below.
http://www.sciencedaily.com/releases/2008/09/080902171151.htm