Mitochondrial damage

Mitochondrial damage is a fundamental and promising area of aging research.

Mitochondrial damage

Feeling Old? Time for a Mitochondrial Tune Up

Halting aging and the development of diseases such as Alzheimer's and Parkinson's may one day be as simple as seeing the doctor for a mitochondrial "tune up."

The tune up, currently in the early stages of development, would repair mutations that occur in mitochondria and are believed to contribute to many afflictions, from diabetes to heart disease.

From biology class, you may remember that mitochondria are the "powerhouses of the cell." These tiny organelles manufacture ATP, which is used as a source of energy. Besides manufacturing ATP, mitochondria are also involved in apoptosis, sending a "suicide" signal to cells.

Mitochondria are unique from other cell organelles because they contain their own DNA. This leaves them susceptible to genetic mutations in the form of DNA damage. Scientists believe that when a cell divides, mitochondria can lose important information, which can contribute to disease and aging.

Correcting defects

To combat this DNA damage, Shaharyar Khan and Rafal Smigrodzki of the University of Virginia are developing a therapy that could potentially prevent mitochondrial diseases and possibly many aspects of aging.

Aging and life extension | Mitochondrial damage | Rafal Smigrodzki

Reduced Mitochondrial Function Important Mechanism In Aging

Scientists at the Karolinska Institute have found that changes in the "powerhouse" of cells, the mitochondria, play a key role in aging. The findings are being published in this week's issue of the journal Nature.

Mitochondria, which provide energy to cells, have their own set of DNA. Mutations of mitochondrial DNA increase with age, but until now no one knew whether this is a result of aging or a cause of aging. New research findings now indicate that the latter is the case.

Mice with a deficient capacity to correct mutations in mitochondrial DNA acquired an increased number of mutations and proved to age considerably earlier than normal. They lived an average of 10 to 12 months compared with the normal 2 or 3 years. These mice also developed several typical signs of premature aging, such as osteoporosis, weight loss, hair loss, anemia, reduced fertility, and heart muscle disorders.

Aging and life extension | Mitochondrial damage

Kurzweil proposes research programs to replace DNA, block bioterror viruses

Ray Kurzweil has proposed a nanobiotechnology research program to replace the cell nucleus and ribosome machinery with a nanocomputer and nanobot to prevent diseases and aging and another program to create defensive technologies against rogue designer viruses.

Kurzweil presented the ideas in a keynote at the recent "Breakthrough Technologies for the World's Biggest Problems" conference on April 28, sponsored by the Arlington Institute.

Aging and life extension | Biotechnology | Biotechnology risk | Bioweapons | DNA damage | Epidemic risk | Health | Mitochondrial damage | Nanotechnology | Neurobiology of aging | Physical enhancement | Ray Kurzweil | Terrorism | Transhumanism

Aeiveos: Mitochondrial Theory of Aging

Excerpt: "This theory originated with Denham Harman proposing that oxidative damage to the mitochondrial DNA results in a loss of energy resources and eventual cell death. Early reviews of the involvement of mitochondria in aging include Strehler, B.L., 1977, pp 243-247 and Miquel, 1980 . Further updates are by Miquel in Miquel, 1982 , Miquel, 1983 and Miquel, 1992 . A major expansion of the ideas of mitochondrial DNA damage theories were provided by Linnane and Ozawa, 1989. They proposed that oxidative damage to the mitochondrial DNA results in a loss of energy resources and that clinical interventions could counteract this process. Evidence would seem to indicate that, with increasing age, there is an increase in DNA damage and a decline in mitochondrial activity (respiratory function) in post-mitotic (non-dividing) cells, e.g. heart and kidney cells. This could result in a shortage of energy which increases the probability of these cell dying in stressful conditions."
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