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Link between hibernation in animals and Alzheimers prevention identified

Research by scientists at the Medical Research Council’s Toxicology Unit, based at the University, has identified a protective mechanism that kicks in when body temperature is lowered, activating a process that prevents the loss of brain cells and the connections between them.

The MRC team led by Professor Giovanna Mallucci (pictured) discovered that this protective process may be defective in neurodegenerative diseases such as Alzheimer’s, contributing to the death of brain cells in these disorders. By simulating the effects of cooling in mice, the scientists have revealed a possible new target for drugs that could protect against neurodegeneration.

In humans, a reduction in body temperature (hypothermia) is known to protect the brain. Cooling leads to the production of a number of different proteins in the brain known as ‘cold-shock’ proteins. One of these, RBM3, has been associated with preventing brain cell death, but it has been unclear how it affects synapse degeneration and regeneration. 

The research has concluded that RBM3 – and perhaps other cold-shock proteins – affects the ability of neurons to regenerate synapses in neurodegenerative diseases, which is essential to prevent synapse loss during disease progression.  The pathway could be a useful target for drugs so that brain cells could be preserved without the need for cooling.

Knowing how these proteins activate synapse regeneration might help scientists find a way of preventing synapse loss, without the need for actual cooling.

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