“A protein released during hypothermia has been found to affect the progression of neurodegenerative disease in mice by sparing neurons from death and preserving the connections between them.”
In the healthy adult brain, synapses are continuously remodeled through a process of elimination and formation. Reduction in synapse number is a consistent early feature of neurodegenerative diseases, suggesting deficient compensatory mechanisms. Although much is known about toxic processes leading to synaptic dysfunction and loss, how synaptic regeneration is affected is not well known. In hibernating mammals, cooling induces loss of synaptic contacts, which are reformed on rewarming, a form of structural plasticity. The authors of this study found that similar changes occur in artificially cooled laboratory rodents. Cooling and hibernation also induce a number of cold-shock proteins in the brain, including the RNA binding protein, RBM3. Deficient synapse regeneration mediated at least in part by failure of the RBM3 stress response, likely contributes to synapse loss throughout the course of neurodegenerative disease. The authors suggest that enhancing cold-shock pathways is a potential protective therapy in neurodegenerative disorders.
Peretti D, Bastide A, Radford H, Verity N, Molloy C, Martin MG, Moreno JA, Steinert JR, Smith T, Dinsdale D, Willis AE, Mallucci GR: RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration, Nature [Epub ahead of print, January 14, 2015; doi:10.1038/nature14142 ].

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