Scientists have come up with a new approach to the treatment of genetically caused premature aging

Geneticists from the Institute of Molecular Oncology in Italy and the Karolinska Institute in Sweden have developed a new method of treating childhood progeria, or Hutchinson-Guilford syndrome, a disease characterized by an accelerated aging process. Experiments on human cell lines and laboratory mice have shown that antisense oligonucleotide therapy can be effective.

Progeria is a rare genetic disease that affects about one person in 18 million. The average life expectancy in this condition is 13 years. 

The reason is a mutation of the LMNA gene, in which the protein progerin disrupting the functioning of cells and leading to accelerated aging is synthesized.

Scientists have long been trying to develop an effective treatment for this disease, but only now they are closer to this goal. 

Swedish and Italian researchers collected cell samples from children with progeria to study telomere dysfunction and the accumulation of telomeric non-coding RNA that is not translated into protein. Experts decided to reduce the level of transcription of such RNA and thereby normalize the process of cell division by adding antisense oligonucleotides - short sequences of nucleic acid that can attach to the RNA molecules of mutant LMNA genes and suppress the synthesis of progerin.

Mice with progeria who received oligonucleotide therapy increased maximum and average life expectancy by 44% and 24%, respectively.

According to the authors, this discovery is extremely important, since such therapy can be useful not only for the treatment of progeria but also for the normalization of aging processes (progerin is also found in the cells of older people). In the long term, such treatment can delay the aging of people who do not suffer from genetic disorders.

In the future, scientists intend to research healthy people to study in more detail the role of this protein in the development of age-related changes.

Nov. 19, 2019, 10:54 a.m.

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