MitoSENS

About MitoSENS

Mitochondria are a component of cells that perform cellular respiration. That is to say, they react oxygen with nutrients from our free radicalfood to produce water, carbon dioxide, and useable energy (in the form of ATP). A side effect of this process is the production of reactive chemical byproducts that damage nearby components of the cell. Mitochondria are unique in that they have their own DNA (mtDNA), separate from the nucleus. Being at the site of cellular respiration, the mtDNA is vulnerable to its reactive byproducts. Worse yet, the mitochondria's capacity for repairing DNA damage is much more limited than that of the nucleus. Mutations to the mtDNA inevitably accumulate leading to dysfunction of mitochondria, and contributing to aging of the organism. The goal of MitoSENS is to obviate mtDNA mutations by expressing the mtDNA genes from the nucleus.

Fortunately, we would be completing a process that evolution has already started.

The mitochondrial genome originally had thousands of genes, but evolution has reduced it to a mere 13 (protein encoding) genes in humans. By studying how nature transfered expression of other genes from the mitochondria to the nucleus, we can identify the necessary steps to transfer the remaining 13 genes (in humans).

MitoSENS research is currently being conducted in the lab of Ian Holt at Cambridge University. To learn more about the MitoSENS strategy from its originator and Methuselah Foundation chairperson Aubrey de Grey, see the SENS website here (laymans terms) or here (technical).
The Research Team

Mark Hamalainen is a researcher for the Methuselah Foundation and a PhD Candidate at Cambridge University. He has previously worked on the LysoSENS project and is now focusing on MitoSENS.

Questions and Contact

Any questions or comments on MitoSENS research can be directed to mark.hamalainen@gmail.com