Mitochondrial Dysfunction and Disease

Mitochondria are the powerhouses of the cell. The better your mitochondria perform, the more energy you will have. All of your cells need well-functioning mitochondria, or they will suffer. Mitochondria were probably bacteria, originally. They contain much of their own DNA, and divide like bacteria, with both copies retaining the genome.

Not surprisingly, mitochondria are sensitive to certain antibiotics, like bacteria. In fact, one approach to cancer chemotherapy is to develop an antibiotic that specifically targets the mitochondria of cancer cells. Causing sufficient damage to mitochondria can induce apoptosis of the cell. A lot of research is currently being conducted to clarify the connection of mitochondria with caspase releae and subsequent apoptosis.

Mitochondrial dysfunction participates in neurodegeneration of Huntington disease (HD), Friedreich ataxia, hereditary spastic paraplegia, and rare familial forms of Parkinson disease (PD), Alzheimer disease (AD), and amyotrophic lateral sclerosis (ALS). Although this is only one of the many molecular pathways to neurodegeneration, it is a potentially important one.

In a previous post, I referred to the speculation that chronic fatigue syndrome was related to mitochondrial dysfunction, which could theoretically be caused by any number of micro-organisms including Epstein Barr Virus (EBV). Chemical insult can also cause mitochondrial dysfunction.

The scope of mitochondrial dysfunction is very broad. Some disorders are inherited and manifest in infancy or childhood, many others are acquired in later life. Several dozen known diseases are related to mitochondrial dysfunction.

The good news is that science is getting a better understanding of how mitochondria resist damage.

The SENS approach to life extension includes the preservation of mitochondrial function as one of its basic tenets.

What if we could all have the mitochondrial function of a Lance Armstrong or a champion Iron Man triathlete? That is the short term goal. Longer term, who knows?