Holding back the march of time means much more than countering wrinkles with Botox injections and trying to keep our assorted bits and pieces from sagging. It means keeping our brains sharp and warding off a plethora of diseases and chronic conditions. And a team of scientists from the University of Nottingham may have just figured out how we can slow down the debilitating effects of aging on our bodies.
The key looks to be a protein found within the powerhouse of a cell, and their research, published in the academic journal Aging, could have special significance for combating age-related decline and halting the progression of neurodegenerative conditions such as Alzheimer's and Parkinson's.
The work, led by Dr. Lisa Chakrabarti and PhD student Amelia Pollard in the University's School of Veterinary Medicine and Science, has centered on a family of proteins called carbonic anhydrase found within mitochondria — the cells' "batteries," which convert the oxygen we breathe into the energy (ATP) needed to power our body.
"What's really exciting about this development is that we have been able to surmise that the function of this protein is playing a role in the aging process within the cell," Dr. Chakrabarti said. "This gives us a very promising start in working out how we can best target this protein within the mitochondria to slow the effects of aging in the body while limiting other unwanted side effects on the body. It could potentially offer a significant new avenue in both tackling degenerative illnesses and the general effects of aging on the body."
Using a specialist process called 2-D gel electrophoresis, the scientists separated out all the proteins found within the mitochondria of brain cells and muscle cells from normal young brains and normal middle-age brains and compared the two samples.
They found that the carbonic anhydrase was found in greater quantity and was more active in the samples of the middle-age brain. Significantly, this increase was also reflected in samples from young brains suffering from early degeneration, suggesting that the increase is detrimental.
To establish whether this was indeed detrimental and not evidence of the body's attempt to guard against this degeneration — known as a protective effect — the scientists studied the effect of carbonic anhydrase on nematode worms.
They found that feeding carbonic anhydrase to the tiny c elegans worms — measuring around just one millimeter in length — reduced their life span.
As we age, our body's tissues and functions begin to diminish. Aging has been associated with a loss of muscle mass, which begins around the age of 50 and becomes more pronounced in our 60s, leading to a reduction in strength and greater frailty.
Aging in the brain can cause the onset of cognitive impairment affecting memory, reasoning and multitasking and can lead to dementia. Other neurodegenerative diseases such as Alzheimer's and Parkinson's can cause the early onset of cognitive decline.
The scientists are continuing their work to identify chemical compounds that may be successful in targeting carbonic anhydrase and to study what effect these potential inhibitors have on worms which have had their lives shortened by the protein.
The Nottingham study could be the first step to the development of a new type of drug that targets carbonic anhydrase in just the body's mitochondria to protect against aging and degeneration.