With an ageing population, neurodegenerative diseases are becoming more prevalent and an effective solution needs to be found fast. The Alzheimer’s Association (AA) in a 2012 report estimated that a new case of will appear every 33 seconds by 2050. In neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease there is a loss in the number of synapses which leads to symptoms such as memory loss.
Researchers at the University of Leicester and University of Cambridge recently published a study in Nature looking at the effects of hibernation on brain synapses on mice. It was found that the lost synapses when going into hibernation were recovered when coming out of it. They next wanted to investigate if the level of protein RBM3 (a protein which is still produced despite cold temperatures) played a role in the regeneration of synapse.
Brains of mice from three groups (normal, Alzheimer’s disease sufferer and prion disease sufferer) were studied during cooling to 16-18C and rewarming (although some were not cooled and had their levels of RBM3 chemically altered as a control), comparing the number of synapses and level of RBM3.
It was found they had increased levels of RBM3 during cooling and it remained elevated for up to three days after. The mice which had been cooled survived for an average of seven days longer which implies cooling gives an added protection. However, those with a more advanced version of the diseases lost synapses when cooled and could not regrow them. In addition, it was found that disease progression sped up when RBM3 levels were reduced.
It was concluded that protein RBM3 is involved in the pathway of synapse regeneration in mice. The research showed how cooling is protective against the loss of synapses in the early stages of rodent forms of Alzheimer’s disease and prion disease but in advanced stages it was suggested that cooling may not be protective due to no increase in the level of RBM3s. It has already been found from other investigations that therapeutic hypothermia leads to increases in RBM3 and if this pathway could be stimulated in humans it may lead to a potential treatment for neurodegenerative disorders but this is at a very early stage.