13 March 2019

A new cause of aging

Aging-causing genetic parasites have been defeated

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Scientists at the University of Rochester in the USA have found out that one of the causes of aging are retrotransposons LINE1 – sections of DNA that can move and multiply within the genome, also called mobile genetic elements (MGE). The researchers were able to suppress their activity in mice, reducing age-related chronic inflammation. This is reported in a press release on Medicalexpress (Selfish genetic elements amplify inflammation and age-related diseases).

Researchers have shown that LINE1 become more active with age, contributing to the development of inflammation and related diseases. Also, over the years, molecular mechanisms that suppress gene expression and regulate retrotransposons become less effective.

It turned out that some copies of LINE1 leave the cell nucleus and enter the cytoplasm. The molecules located there, which provide protection against viruses and their DNA, recognize retrotransposons and cause a "false alarm" in the form of inflammatory reactions. When the researchers reduced the activity of LINE1 in mice using reverse transcriptase inhibitors – an enzyme that provides copying of genetic elements – the animals' health improved and inflammation decreased.

The drugs used in the scientific work were originally developed to suppress reverse transcriptase in the cells of people infected with HIV. The virus uses an enzyme to insert its genes into the genome of an infected cell. It is expected that this therapy should help in the fight against pathological conditions caused by inflammation, including neurodegenerative and autoimmune diseases.

LINE1 retrotransposons are the most common genetic parasites in the human genome, which make up approximately 20 percent of human DNA. They do not have any useful function, but they are able to copy and insert new copies into the host genome. They are known to lead to chromosome instability and cancer.

Article by Simon et al. LINE1 Derepression in Aged Wild-Type and SIRT6-Deficient Mice Drives Inflammation is published in the journal Cell Metabolism.

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