Mitochondria supply 90% of the energy needed by our cells and regulate a variety of biological functions including cell death. Invariably, mitochondrial dysfunction can lead to the onset of a range of neurodegenerative diseases by compromising energy production. Thus, there is a critical need to develop therapeutic strategies which can correct mitochondrial dysfunction by stimulating ATP production in these diseased cells.

 

Mitochondria contains its own small genome (mtDNA), which comprises genes that encode for proteins associated with ATP production. Mitochondrial dysfunction occurs where one or more of these genes contains defects (i.e.,mutations called Single Nucleotide Polymorphisms or SNPs), resulting in reduced ATP production. Diseases related tomitochondrial dysfunction arise when these SNPs result in ATP production falling below a critical threshold.