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Chilling Facts: How Cold Can Improve Longevity and Ward Off Aging-Related Diseases

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Cold activates a cellular cleansing mechanism that breaks down harmful protein aggregates responsible for various diseases associated with aging.

And in recent years, studies of various model organisms have already shown that life expectancy increases dramatically with a decrease in body temperature. However, how exactly this works remains unclear.

According to an article published in the journal Nature Aging, a research team from the CECAD Center of Excellence in Aging Research at the University of Cologne has discovered one of the responsible mechanisms.

Professor David Vilches and his team used a non-vertebrate model of the nematode Caenorhabditis elegans and cultured human cells in the laboratory.

Both carry genes for two neurodegenerative diseases that commonly occur in old age: amyotrophic lateral sclerosis (ALS) and Huntington’s disease.

Both diseases are characterized by the accumulation of harmful protein deposits in the form of so-called pathological protein aggregates. In both model organisms, cold effectively removed protein clumps, thereby preventing pathological protein aggregation in both ALS and Huntington’s disease.

More precisely, scientists have discovered the effect of cold on the activity of proteasomes, a cellular mechanism that removes damaged proteins from cells.

The results showed that cold temperature (15°C) selectively stimulates the PA28γ/PSME3 proteasome activator, which attenuates aging-induced deficiency in both nematode and human cells. In both cases, proteasome activity could be activated by a slight decrease in temperature.

“Together, these results show how cold has maintained an evolutionary impact on proteasome regulation with therapeutic implications for aging and age-related diseases,” explained Professor Vilches.

Aging is a major risk factor for a number of neurodegenerative diseases associated with protein aggregation, including Alzheimer’s, Parkinson’s, Huntington’s and amyotrophic lateral sclerosis. “We believe these results can be applied to other age-related neurodegenerative diseases as well as other animal species,” Vilches added.

The key finding was that proteasome activity could also be increased by overexpressing the promoter gene. In this way, disease-causing proteins can be eliminated even at a normal body temperature of 37°C. These discoveries could become therapeutic targets for the treatment of aging and age-related diseases.

Source: Medical Express

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