Dementia features an early and currently irreversible loss of neuronal connections essential for brain function. Hibernating animals can regenerate these connections after a bout of hypothermia during hibernation. By cooling mice modelling dementia, our group mimicked hibernation and observed dramatic improvements in outcomes. They then identified a key protein regulating this effect. In my PhD, I have discovered a neuronal cold sensor which, when targeted with a drug, induces this protein without cooling. This drug increases survival in a mouse model of dementia. This could represent a novel treatment for dementia and other diseases where cooling is used for neuroprotection.
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