The body’s decline as we get older or illnesses such as Alzheimer’s caused by ageing could be slowed or stopped after a breakthrough by British scientists. Scientists at Nottingham University discovered a protein found within the powerhouse of a cell has a crucial role in the ageing process.
The discovery could lead to new drugs to slow the debilitating effects of ageing on our bodies or halt the progression of neurodegenerative conditions such as Alzheimer’s and Parkinson’s Disease. As we age, our body’s tissues and functions begin to diminish. Loss of muscle mass begins around 50 and becomes more pronounced in our 60s, leading to a reduction in strength and greater frailty.
Ageing 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 Disease can cause the early onset of cognitive decline. The study focused on a family of proteins called carbonic anhydrase found within mitochondria, which convert the oxygen we breathe into the energy (ATP) needed to power our body.
Dr Lisa Chakrabarti, biochemistry lecturer in the University’s School of Veterinary Medicine said:
“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 ageing process within the cell.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 ageing 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 ageing on the body.”
Using a specialist process called 2D gel electrophoresis, the study separated out all the proteins found within the mitochondria of brain cells and muscle cells from normal young brains and normal middle-aged brains. These were then compared and it was found the carbonic anhydrase were in greater quantity and was more active in the samples of the middle-aged 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 - it studied the effect of carbonic anhydrase on nematode worms. Feeding carbonic anhydrase to the tiny c elegans worms - measuring around just one millimetre in length - reduced their life span. The next step is 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 ageing and degeneration.
The study was published in the journal Aging.