'Hibernation protein' could help repair dementia damage

Conclusion The researchers have shown how cooling is protective against the loss of synapses in the early stages of rodent forms of Alzheimer's disease and a form of prion disease. Cooling also increased how long prion-infected mice survived. But cooling was not protective in the later stages of the diseases. The researchers found this may in part be because of the protein RBM3, which is stimulated during cooling. They found levels of RBM3 increased in the early stages of the diseases when the mice were cooled, but did not in the later stages. Stimulating this protein without cooling the mice also slowed down the loss of synapses and improved survival in mice with a prion infection. The results also showed the disease processes sped up when RBM3 levels were reduced. The researchers say this indicates RBM3 is likely to be involved in the maintenance of synapse connections under normal conditions, not just during hibernation. It is already known from other studies that similar increases in RBM3 occur when humans are given therapeutic hypothermia, where the body temperature is reduced to 34C as a protective treatment – for instance, after a heart attack. It may be the case that if this pathway is stimulated in humans, it could be a new avenue of research for the treatment of neurodegenerative disorders such as Alzheimer's disease. This is intriguing research, but still very much in its early stages. There is much we don't know about Alzheimer's disease and other related ...
Source: NHS News Feed - Category: Consumer Health News Tags: Neurology Source Type: news