Critical Step in DNA Damage Pinpointed – Immortality Within Grasp?

Critical step in DNA repair identified. Can it lead us to immortality? Image source: Shutterstock
AGING – THE NATURAL PROCESS

Aging is inevitable, just like an extra candle on your birthday cake. It is the accumulation of gradual changes over time – which has a good face of wisdom and maturity; a bad face of minor wrinkles; and an ugly face of severe disorders like Alzheimer’s and Parkinson’s disease.

Not only that but from time immemorial, humans have always wanted to be immortal.  Almost craving for the fountain of youth or perhaps slowing down aging.

With the advancements in scientific technologies and innovations, Scientists have turned their focus on what causes aging rather than finding the fountain of youth.

THE GIANT LEAP

This is where scientists from the University of New South Wales (UNSW) made a magnificent discovery.  In the paper published in Science, they have explained the molecular basis of reversing aging through the cellular DNA damage repair mechanism. Consequently, this could bring potential solutions to extend life expectancy.

Although our cells have an innate DNA damage repair mechanism, it tends to lose its efficiency as we grow older. However, the scientists have identified oxidized nicotinamide adenine dinucleotide (NAD+) as a key molecule in restoring the DNA damage repair mechanism.

Can we reverse dna damage which causes aging?
The natural clock of aging. Image credits: Fotolia/rolffimages

The specific binding of NAD+ to the Nudix homology domain (NHD) of DBC1 protein restricts its interaction with a crucial DNA repair enzyme, Poly (ADP-ribose) polymerase 1 (PARP1), which in turn restores the normal functioning of PARP1.

NAD+ is a metabolic sensor present abundantly in the cells. Nonetheless, the levels decline with age. Scientists introduced precursor of NAD+, nicotinamide mononucleotide (NMN) in old mice.

Upon receiving NMN, old mice showed a profound increase in NAD+ levels and PARP1 activity. This led to a marked decrease in DNA damage biomarkers, which altogether represents improved DNA repair management.

Moreover, the treatment with NMN also provided protection against radiation-induced DNA damage, as observed by exposing NMN pre/post-treated mice with radiation.

The cells of the old mice were indistinguishable from the young mice, after just one week of treatment,” says Prof. David Sinclair of the UNSW School of Medical Sciences and Harvard Medical School Boston, the lead author of the present study.

“Our results unveil a key mechanism in cellular degeneration and aging but beyond that they point to a therapeutic avenue to halt and reverse age-related and radiation-induced DNA damage”, says Prof. David Sinclair.

HUMAN TRIALS

However, there are huge biological differences between mice and humans. Therefore, affirmations are required from further animal and human studies before proceeding towards therapeutic interventions.

Professor Sinclair and Dr Wu have been working on making NMN into a drug substance. This could be with their companies MetroBiotech NSW and MetroBiotech International.

The human trials will begin this year at Brigham and Women’s Hospital, in Boston.

This is the closest we are to a safe and effective anti-ageing drug that’s perhaps only three to five years away from being on the market if the trials go well,” says Prof. David Sinclair.

BENEFICIARIES OF THE THERAPY

The therapeutic intervention that can potentially reverse aging definitely brings hope for all of us. Most of all the beneficiaries of the therapy could be the one who is more susceptible to age-related changes.

Of note, frequent flyers can be benefited by the same therapy as well.

The other population that can benefit from this work is the cancer patients who are susceptible to DNA damage due to radiation therapy.

Not only this, the study has possible suitors in NASA, which is counting on the NMN therapy for keeping astronauts in good health during a four-year mission to Mars.

We are definitely on fast track to immortality.

Source UNSW Science

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