Recently another paper was produced which hinted at a link between mitochondrial DNA damage and aging. In fact I have been of the view for some time that the damage to mitochondrial DNA is what drives both aging and development at the lowest level. I have said this before, but thought a summary would be useful. It is worth, however, explaining a few terms first before going into the details of how this happens. It is well known that animals (including people) are made of large number of cells. Within those cells there are little "organelles" called mitochondria that are used to convert nutrients into ATP (Adenosine Tri Phosphate) which is used by cells as a form of energy. There is a hypothesis that is generally believed to be true that this structure of cells arose from some bacteria going into old cells called archea as it created a form of symbiosis where the larger cells provided nutrients to the bacteria for the bacteria to process those. This is called Endosymbio...
The idea that Parkinson's Disease (PD) is an accelerated form of brain aging has been around for quite a long time. However, as with aging more generally any hypothesis as to the mechanisms behind Parkinson's needs to explain all the known research data. I have been discussing PD with a number of people over the past few months. The results from research indicate that Parkinsons is not primarily caused by genetic factors. That is because there are studies where individual twins get Parkinsons, whilst their twin does not. I was wondering, therefore, what might be an alternative cause. This paper is one that substantiates the argument that normally the brain does not age as fast as the rest of the body. What we need to look at is what might cause this to happen. If we start with the assumption from my previous posts that aging results from the mutation of mitochondrial DNA (mtDNA) then we need to find something that prevents the mutation of mtDNA in the brain that does n...