Ice baths and cold therapy are becoming increasingly popular, and for good reason. Cold offers a variety of health-promoting effects such as anti-inflammation, pain relief, muscle regeneration, stress reduction and strengthening of the immune system. Now there is also new hope in dementia research: the so-called cold shock protein RBM3, which is increasingly produced at low temperatures, shows astonishing neuroprotective properties. But can cold really be the key to treating dementia?
What is the cold shock protein RBM3?
The cold shock protein owes its name to the fact that it is increasingly produced when exposed to cold, even though protein synthesis and metabolism are downregulated under such conditions. The RBM3 protein is found in a variety of organisms, including insects, amphibians, fish, birds, plants and especially mammals, including humans.
Particularly striking is the strong expression of RBM3 in certain areas of the hippocampus, a region of the brain that forms the episodic memory and which is affected first in Alzheimer’s disease. In the hippocampus, the cold shock protein plays an important role in cell proliferation and cell specialization. A high release of RBM3 was also detected in newly formed nerve cells . In this way, RBM3 could represent a protective protein for the vulnerable hippocampus region.
The role of RBM3 in the brain
Using cell culture and animal studies, scientists have discovered that RBM3 can have a neuroprotective effect via various mechanisms.
On the one hand, the protein can maintain self-renewal and the formation of neuronal stem and progenitor cells and thus preserve the total number of neuronal cells. RBM3 also influences the functions of nerve cells by improving the processes necessary for protein formation (transcription and translation). It is also able to modulate the number of synapses (connection points of nerve cells), reorganize synaptic connections and counteract the loss of synapses. In addition, RBM3 can reduce the self-destruction of nerve cells and inhibit certain enzymes that are responsible for the formation of ß-amyloid plaques . This could mechanistically explain the preventive effect of RBM3 against neurodegeneration.
Cold shock protein meets Alzheimer’s research
It has long been known that a reorganization of synaptic contacts (a form of structural plasticity) takes place during hibernation in mammals. This phenomenon could now also be induced in rodents by artificial hypothermia and rewarming. During hibernation and artificial exposure to cold, a number of cold shock proteins are also produced in the brains of these animals, including RBM3.
Based on this knowledge, researchers at the University of Cambridge exposed prion-infected mice (which develop Alzheimer’s-like disease) and genetically modified Alzheimer’s mice (which develop familial Alzheimer’s disease) to hypothermia. After the cold exposure process, the mice had time to warm up again. The researchers came to some exciting conclusions:
In both mouse models, it was possible to stop the premature loss of synapses that would normally occur due to their disease (prion infection or Alzheimer’s disease). The ability of the synapses to regenerate after cooling correlated clearly with the loss of the ability to release RBM3. Increased formation of RBM3 in the hippocampus preserved the ability to regenerate synapses after cooling, while failure of the RBM3 stress response could no longer compensate for synaptic losses .
The researchers were thus able to show that an increase in RBM3 in response to cold exposure leads to sustained synaptic protection in both Alzheimer’s mice and prion-infected mice. This prevented behavioral deficits and neuronal losses and significantly extended the survival time. In contrast, the lack of RBM3 formation enhanced synaptic loss in both animal models, accelerated the disease and prevented the neuroprotective effects of hypothermia. The authors conclude that insufficient synapse regeneration, which is apparently also mediated by the failure of the stress response of RBM3, leads to reduced structural plasticity. This in turn can lead to the loss of synapses and thus to neurodegenerative diseases .
If you would like even deeper scientific insights into these studies, you can watch the video contribution of theresearch group to watch it.
The increased production of the cold shock protein RBM3 through exposure to cold shows promising results in cell culture and animal studies with regard to the protection of nerve cells and synapses. These positive results suggest that cold therapy could also be a protective treatment for neurodegenerative diseases in humans with few side effects. Even if the transferability of these studies to humans is not yet certain, there are now numerous indications from empirical medicine that exposure to cold can also have enormous health benefits for the human organism. Simply start with alternating showers or two minutes of cold showers every day!
In connection with ice bathing, a conversation between Prof. Spitz and Dr. Matthias Wittfoth is also worth seeing and hearing on the subject of Cold & breathing as an elixir of life as an elixir of life.
With this ice-cold newsfeed, the ‘Knowledge stops Dementia’ team says goodbye to you for this year and would like to thank you for your loyalty and support in 2023!
We wish you a merry and blessed Christmas and
Good luck and, above all, continued good health in 2024!
Hu, Y., Liu, Y., Quan, X., Fan, W., Xu, B., & Li, S. (2022). RBM3 is an outstanding cold shock protein with multiple physiological functions beyond hypothermia. Journal of Cellular Physiology, 237(10), 3788-3802.https://doi.org/10.1002/jcp.30852
- Peretti, D., Bastide, A., Radford, H., Verity, N., Molloy, C., Martin, M. G., Moreno, J. A., Steinert, J. R., Smith, T., Dinsdale, D., Willis, A. E., & Mallucci, G. R. (2015). RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. Nature, 518(7538), 236-239.https://doi.org/10.1038/nature14142
Photo by Mika Ruusunen on Unsplash