Follow
Scientists from Medical Research Council Toxicology Unit at the University of Leicester identified a mechanism at a molecular level that protects the brain cells when the core body temperature falls. This process was found to have an impact in protecting against neurodegeneration in mice.
The communication of the neurons takes place with the help of synapses. These junctions are fluid. They form as a response to damage, activity or environmental changes. Neurodegenerative diseases like Alzheimer’s or prion diseases like Creutzfeldt–Jakob disorder can trigger the loss of synapses.
According to the researchers’ results, hypothermia or hibernating mammals, events when it is recorded a drop in body’s core temperature the brain activity gets slower and synapses break down. When the temperature of the mammals returns to normal values, synapses have the ability to regenerate and the brain activity returns to full capacity.
In this process molecular events were also studied by researchers and RBM3 protein was standing out. RBM3 protein was getting activated when low temperatures threatened the nerve cells. It had another effect: when the body recovered the protein triggered synapses’ regeneration process.
The researchers asked a simple question: in absence of body temperature drop, can the RBM3 protein protect brain cells against neurodegeneration? They altered the levels of the protein to see how this can be of any help to answer the question.
A study was undertaken on mice whose body temperature was altered to simulate the hibernating of other mammal species. For 45 minutes the mice’s temperature was decreased to 16-18ºC. Synapses mostly from the brain’s memory area fell when the temperature dropped, but the regeneration process started when the mice recovered.
They repeated the experiment with mice having indication of brain neurodegeneration similar to prion diseases or Alzheimer’s. In these animals the protein did not kick-start the recovery process when their body temperature went back to normal. This suggests that protein RBM3 is an essential factor in regenerating and protecting the synapses.
Then RBM3 levels were boosted in mice with brain degeneration problems and the nerve cells were experiencing protection and a slow in memory difficulties.
The research study’s results suggest that these findings can be used to develop a new range of treatments against brain degeneration diseases like Alzheimer’s.
Image Source: Medical Xpress
