A Cologne research group has discovered that cold prevents the clumping of proteins and thus also typical neurodegenerative diseases of old age such as ALS and Huntington’s disease.
It has been known for some time that a lower body temperature can lead to a longer life. Of course, one should not overdo the reduction in temperature, but a moderate reduction can have very positive effects on lifespan. This was found in cold-blooded animals such as worms, flies or fish, as well as in warm-blooded animals such as mammals.
The nematode, for example, lives much longer if it has a body temperature of 15 degrees Celsius instead of the normal 20 degrees Celsius. And in mice, a slight drop in body temperature of just 0.5 degrees Celsius extends lifespan significantly.
Always cooler, always older
Studies have also reported a correlation between body temperature and lifespan in humans. The normal human body temperature is between 36.5 and 37 degrees Celsius. A sharp drop in body temperature below 35 degrees Celsius leads to hypothermia, so it would not be helpful. However, human body temperature fluctuates slightly during the day and even reaches a cool 36 degrees Celsius during sleep.
And a previous study even shows that human body temperature has fallen steadily by 0.03 degrees Celsius per decade since the Industrial Revolution, suggesting a possible link to the progressive increase in human life expectancy over the past 160 years.
Attack on clumping proteins
But how could this connection come about? A research group from the CECAD cluster of excellence in aging research at the University of Cologne has now taken a big step forward in answering this question. The team deciphered a mechanism that provides a possible explanation.
The researchers around Prof. Dr. David Vilchez examined the nematode Caenorhabditis elegans and also cultivated human cells. Both carried the genes for two neurodegenerative diseases that typically appear with age: amyotrophic lateral sclerosis (ALS) and Huntington’s disease. The diseases are characterized by accumulations of harmful protein deposits, so-called pathological protein aggregations. In both model organisms, cold caused the proteins that tend to clump to be actively removed and pathological protein aggregation to be prevented.
We believe that these results can also be transferred to other age-related neurodegenerative diseases.
Prof. David Vilchez, University of Cologne
Aging is a major risk factor for several neurodegenerative diseases associated with protein aggregation, including Alzheimer’s, Parkinson’s, and even Huntington’s and ALS. David Vilchez says: “We believe that these results can be extrapolated to other age-related neurodegenerative diseases, as well as to other animal species.”
Another central finding of the research work is that the activity of the so-called proteasome activator can also be increased through genetic overexpression. In this way, disease-causing proteins can be eliminated even at a normal temperature of 37 degrees Celsius. This results in possible starting points for therapeutic interventions in aging and age-related diseases.
As is so often the case, much more research needs to be done, but a start has been made.
The Study “Cold temperature extends longevity and prevents disease-related protein aggregation through PA28γ-induced proteasomes” is in the journal Science Aging appeared
This topic in the program:The First | BRISANT | March 27, 2023 | 5:15 p.m