Skip to main content

Posts

Showing posts from June, 2025

The effects of mitochondrial DNA damage on neurons

Obviously when mtDNA is damaged in neurons that can have various effects depending on the damage. A key point, however, is that if there is a process which is damaging mtDNA then if that continues then the mtDNA will get further damaged. As some relatively minor damage appears to be caused by the replication of mtDNA itself then it is like there is a very slow moving footpath moving towards cell failure. Hence when looking at how to rectify this then certain points need to be made. When mtDNA is damaged this will not immediately affect the structure of the cell. What it does is to change how the cell produces or fails to produce proteins in the future. Hence if the process of mtDNA damage stops, the cell is unlikely to be in its stable state and can be expected to deteriorate in function to a point at which homeostasis is achieved. It is hard, but possible, to improve mtDNA. However, that will not immediately improve the function of the cell and it may need a stimulus to rege...

Transitions, Transversions and Deletions in mitochondrial DNA and their relevance to Parkinsons, ALS/MND and Aging.

I aim to write this blog so that people don't need a detailed understanding of genetics to read it. I assume people know that genetics involves DNA being used to produce proteins. DNA is comprised of four nucleotides. Two of these are purines Adenine (A) and Guanine (G). The other two are pyrimidines Thymine (T) and Cytosine (C). They pair in two pairs A to T and G to C. Each pair is called a base pair. To produce a protein they are copied to mRNA (messenger RNA) which is then used by the ribosome to create proteins. There is DNA in the nucleus of the cell and there is also DNA in the mitochondria (the little chemical factories that generate ATP and other molecules used by the cell). There is a three base pair code (identifying which amino acid to use) used to convert DNA into protein (via mRNA). Interestingly the code is slightly different in the nucleus/ribosome to the mitochondria. So far so good. DNA can be mutated where one nucleotide for some reason or other is ch...

Follicular Atresia and Mitochondria - Is this how the ovary picks the best egg with the best mitochondria?

I wrote previously about how babies are born young. The essence is that for youth you need efficient mitochondria with a high membrane potential (when running in a steady state generating ATP). When an egg is created it is created with a mitochondrial bottleneck. This reduces the variation in mitochondrial DNA (mtDNA) to about 3 copies (according to recent research). However, this does not as far as research indicates select for better mtDNA (and hence more efficient mitochondria). Relatively few babies are born with mitochondrial disease because the eggs don't get fertilised, don't start replicating, don't implant into the uterine wall or miscarry. This is not the only reason for non-viability, but it is a reason. This is seen in how older eggs tend to be less viable. However, there is another selection process for eggs which is called "Follicular Atresia". Follicular Atresia is a really interesting process and the Wikipedia article that I link to does ...