A supporter asks: Everyone knows that mitochondrial free radicals are a key driver of aging, and antioxidants don’t seem to offer any protection. Birds are supposed to have very clean-burning mitochondria, so should you maybe try to cut them off at the source by re-engineering our mitochondria to be more like those of birds?
A supporter asks if “backing up” copies of the mitochondrially-encoded genes in the nucleus is really viable, granted free radical damage in the nucleus. We emphasize the many additional ways that the nuclear copies will be safer than the mitochondrial originals, that the “backup copies” can be backed up again, and how they and additional strategies will buy us time for even better solutions.
Aging muscles lose strength above and beyond what would be expected from the mere loss of muscle mass. Accordingly, many drugs have been shown to stimulate muscle growth in older people, but the increased muscle mass consistently fails to translate into increased strength and physical function. To let people live independent lives for longer, we need damage-repair longevity therapeutics to repair the cellular and molecular damage that makes aging muscle dysfunctional.
The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age. Testing potential therapies for use in humans requires a robust testing …
The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age. The Goal The team is creating a drive to implant new …
The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age. The most prevalent and dangerous types of mutations are the large …
A supporter asks us to elaborate on projects other than allotopic expression (AE), that SRF has undertaken that are targeting mitochondrial dysfunction; and how they relate to the original strategy of allotopic expression?
A supporter asks about how the central MitoSENS strategy can be delivered to our cells.
Week Two of our 2022 End of Year Campaign features MitoSENS (Preventing Damage from Mitochondrial Mutations) – with a disease focus on Challenging Sarcopenia. Also featuring videos from Life Noggin, AMA with Dr. Amutha Boominathan and Michael Rae.
Research Info Mitochondria perform and support several vital functions in a cell, and the alternate genome, mtDNA, plays a critical role in organelle maintenance. There is increasing evidence that mitochondrial function declines with age, and that dysfunctional mitochondria adversely contribute to several metabolic and neuromuscular diseases. Our goal is to address age-acquired and inborn errors …
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