The Mitochondrial Hypothesis of Ageing

In one of our studies we compared post mortembrain sections of Parkinson patients with samples of healthy control subjects of the same age. By staining the samples, we were able to see that a lotof cells in the Substantia nigra had a mitochondrial function disorder. These cells were extracted by laser microdissection to examine their respiratory chain and mtDNA. This examination revealed a high proportion of mutations (deletions) of the mtDNA.

We then compared a large amount of cells of the Parkinson group and the control group and found a significantly higher number of deletions in the Parkinsongroup – a great deal more than was thought in the past, in fact. It has been known for 20 years that there are changes in the mtDNA, but we always thought it was a matter of a few per cent. With single cell technology we were able to prove that 50 to 60 per cent of the mtDNA in Parkinson patients is damaged, which leads to a drastic energy deficit in the affected cells.

What surprised us was that there were a lot of mutations in 60 to 70-year-old control patients as well – although distinctly fewer than in the Parkinson group. In a second step we therefore examined control samples of people of all ages, from a few months to a hundred years old. We found that the mtDNA deletions increase with age. We are born with noor extremely few deletions and at some stage in our life the critical threshold of 50 to 60 per cent of mutations is reached.

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