8:26:52 
2023-04-06 
565
Study: Cold helps to prolong life and prevent diseases associated with aging
The cold activates the cellular cleansing mechanism that breaks down harmful protein aggregates responsible for various diseases associated with aging.
And in recent years, studies of different model organisms have already shown that life expectancy increases dramatically when body temperature decreases. However, exactly how this works remains unclear.
A research team at the University of Cologne's CECAD Center of Excellence in Aging Research has uncovered one of the responsible mechanisms, according to the paper published in the journal Nature Aging.
Professor David Vilches and his team used a non-vertebrate model organism, the nematode Caenorhabditis elegans, and cultured human cells in the laboratory.
Both carry the 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 so-called pathologic protein aggregates. In both model organisms, cold effectively removed protein clumps, thus preventing pathological protein aggregation in both ALS and Huntington's disease.
More precisely, scientists discovered the effect of cold on the activity of proteasomes, a cellular mechanism that removes damaged proteins from cells.
The results revealed that cold temperature (15 °C) selectively stimulates the proteasome activator PA28γ/PSME3 that attenuates senescence-induced deficits in both nematode and human cells. In both cases, the activity of the proteasomes could have been activated by a mild decrease in temperature.
"Together, these results show how cold has maintained an evolutionary impact on the regulation of proteasomes, with therapeutic implications for aging and age-related diseases," explained Professor Vilches.
Aging is a major risk factor for several neurodegenerative diseases associated with protein aggregation, including Alzheimer's, Parkinson's, Huntington's, and amyotrophic lateral sclerosis. "We believe that these findings can be applied to other age-related neurodegenerative diseases as well as to other animal species," added Vilches.
The key finding was that proteasome activity can also be increased by overexpression of the promoter gene. In this way, disease-causing proteins can be eliminated even at a normal body temperature of 37°C. These findings may provide therapeutic targets for aging and age-related diseases.
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