MitoSENS: Preventing damage from mitochondrial mutations
Accumulation of mutations in mitochondrial DNA is recognized as
a significant consequence of aging and is implicated in the
metabolic derangement of aging and in accelerating the course of
the degenerative aging process as a whole. Mutations in the
mitochondrial genes occur as a consequence of constant exposure
to reactive oxygen species resulting from the mitochondrial
energy generation process. Because mitochondria lack an
efficient repair mechanism, these mutations accumulate over time
and compromise respiratory chain function and hence energy
generation. One need only look at the mitochondrial genetic
diseases to see the similarities to many of the diseases and
maladies of aging. For example, mutations in ND1 have been
implicated in the development of Parkinson’s disease, and
Cytochrome B (CYB) mutations can cause muscle fatigue/ exercise
intolerance in young patients. The essential strategy we are
using in our approach to MitoSENS is to render the