Forget cosmetics. Scientists have already succeeded in reversing premature aging

ZAP // Rawpixel, Pixabay

A team of scientists has succeeded in reversing premature aging by preventing the loss of nuclear architecture.

THE Werner syndrome and Hutchinson Gilford Progeria Syndrome are two examples of rare genetic diseases known as progesterone syndromes that cause signs of premature aging in children and young adults.

Patients with progesteroid syndromes have conditions and symptoms that are often related to agingincluding osteoporosis, cataracts, heart disease and type II diabetes.

This aging is characterized by the progressive loss of nuclear architecture and for one genetic program specific to the underlying tissues, but the causes are unclear. on a new studyscientists have discovered a new potential target for the treatment of these syndromes thanks to prevention of the loss of nuclear architecture.

The target is known as nuclear element-1 (L1) RNA, a family of repeat sequences that makes up about 17-20% of the mammalian genome and whose functions are largely unknown.

The DNA architecture known as heterochromatin renders these sequences inactive. There is evidence that heterochromatin depletion during normal aging is related to its Activation.

“Based on theoretical considerations, we understand that a molecular interaction between the L1 RNA and a specific enzyme which controls the stability of heterochromatin could be the cause of the premature aging in progeria syndromes,” explained the researcher at the University of Science and Technology (KAUST) Francesco Della ValleQuoted by Daily SciTech.

The sequencing studies carried out by the KAUST and American teams revealed a higher expression of L1 RNA in cells taken from people with progesteroid syndromes.

Further research revealed that the increased expression of L1 RNA was responsible for the deactivation of an enzyme known as SUV39H1which led to the loss of heterochromatin and in changes in gene expression that promote cellular aging.

Researchers managed to block L1 RNA expression and reverse the aging process in cells taken from patients with progeroid syndromes and in mice that are genetically modified to simulate premature aging.

They did this using short chains of synthetic nucleotides called antisense oligonucleotides (ASO), which specifically target and lead to the degradation of L1 RNA.

Your ASO L1 has been modified to improve its ability to enter and stay stable inside cells. Blocking L1 RNA in cells restored heterochromatin and fought age-related genes. ASO L1 also extended life of progeria-like mice.

Further research should determine whether other mechanisms, acting in parallel with SUV39H1 inhibition, may compromise heterochromatin stability in progeria syndromes.

“Among other findings, our work establishes an important rule”, specifies the bioscientist Valerio Orlando.

“TO contrary to what we thought Previously, aberrant L1 RNA expression is not a consequence of the onset of aging, but a cause of the same, at least in progeria. And now, for the first time, we’re reporting a specific goal rather than an overall goal that acts as a factor. essential getting old,” he explains.

“Given the similarities between progeroid syndromes and diseases associated with chronological aging, investigating and knowing RNA LINE-1 can be a effectively to treat progeroid syndromes, as well as other aging-related diseases characterized by aberrant expression of LINE-1, such as neurodegenerative, metabolic and cardiovascular diseases, and cancer,” says Orlando.

“This study paves the way for new strategies that we think we can help extend human lifespan,” he concludes.

Zap //

Add Comment