Researchers from the CECAD Cluster of Excellence in Aging Research at the University of Cologne (Germany) have discovered that cold Activates a cellular cleansing process that helps break down harmful protein aggregates responsible for causing age-related diseases. This research, published these days in Nature Agingadds to previous studies carried out in different organisms that have shown that the reduction in body temperature can significantly increase life expectancy. Although there are still many unanswered questions about it, this research team has unlocked a key mechanism responsible for the process.
It is known that the extremely low temperatures they can be harmful to organisms, but it has been found that a moderate reduction in body temperature can have very beneficial effects. This phenomenon has been observed in cold-blooded animals such as worms, flies and fish, whose body temperature varies depending on the environment. However, it also applies to mammals, which maintain their body temperature constant regardless of the ambient temperature, whether their environment is hot or cold. For example, a nematode lives longer at a temperature of 15 degrees Celsius than at 20 degrees Celsius. In mice, just a 0.5 degree drop in body temperature can significantly extend their lifespan. All this suggests that the reduction of body temperature is an evolutionary mechanism that plays a key role in the longevity of animals and is conserved in several species.
It has been observed that body temperature in humans is also related to the Life expectancy. Normally, the human body temperature is in the range of 36.5 to 37 degrees Celsius, and it fluctuates slightly during the day, even decreasing to 36 degrees during sleep. Although a sudden drop in body temperature below 35 degrees can cause hypothermia, a curious previous study suggested that a gradual decrease of 0.03 degrees Celsius per decade since the Industrial Revolution could be linked to the progressive increase in life expectancy human in the last 160 years.
Results of the work on the effect of cold on the longevity of organisms
He Dr. David Vilchez and his team used a non-vertebrate model organism known as Caenorhabditis elegans, together with the culture of human cells that contained the genes of two neurodegenerative diseases typical of old age: amyotrophic lateral sclerosis (ALS) and Huntington’s disease. These diseases are characterized by the accumulation of deleterious and harmful protein deposits, also known as pathological protein aggregations. The use of low temperatures in both model organisms allowed for the active removal of protein clumps, which prevented the pathologic protein aggregation that is common in both ALS and Huntington’s disease.
The scientists investigated the effect of low temperatures on the activity of proteasomes, which are the cellular mechanisms responsible for removing damaged proteins from cells. During the study, the proteasome activator PA28γ/PSME3 was found to decrease ageing-related deficits in nematode and human cells. In addition, it was found that proteasome activity can be increased by a moderate decrease in temperature in both organisms. Professor Vilchez concluded that these results indicate that cold has maintained its ability to regulate the proteasome throughout evolution, which has therapeutic implications for aging and aging-associated diseases.
Aging has been identified as a major risk factor for several neurodegenerative diseases involving protein aggregation, such as Alzheimer’s, Parkinson’s, Huntington’s disease, and ALS. Professor Vilchez indicated that: “We believe that these results can be applied to other age-related neurodegenerative diseases, as well as to other animal species.” A key finding was that proteasome activity can be increased by gene overexpression of the activator, allowing the clearance of disease-causing proteins even at normal body temperatures of 37 degrees Celsius. These results offer potential therapeutic targets for aging and age-related diseases.