According to Cambridge University research, there exist “cold shock” proteins that manifest themselves in wintertime swimmers following increased exposure to cold water.
Researchers say the protein, called RBM3, shows promising signs of slowing the onset of dementia and even repairing damaged synapses as a result of the disease.
Synapses serve as the connections between cells in the brain and are heavily targeted by dementia.
Professor Giovanna Malluci, head of the UK Dementia Research Institute’s Centre at the University of Cambridge, and her team have noticed that during winter, animals are able to preserve their synapses during hibernation and regenerate them after waking up for the spring.
In different laboratory tests with mice, the RBM3 protein was able to prevent vulnerable synapses from being severed, showing further signs that it can be used as a shield against dementia related diseases.
The research team believes that in order for people to create this protein naturally, their body temperature must reach hypothermic levels, below 95 degrees Fahrenheit.
Along with winter swimmers, research has been done with babies and heart and stroke patients where levels of RBM3 were found after lowering their body temperatures to the necessary levels.
Increasing exposure of dementia patients to cold water could provide crucial findings; however, the risks of overexposure, such as heart attack or stroke in people with high blood pressure, offset the benefits of a dementia treatment.
Applying this concept to humans, artificial creation of the RBM3 protein is needed for safe examination of the possible effects on non-swimmers.
More than 5 million Americans age 65 and older are living with some level of Alzheimer’s dementia in 2020. 80 percent of those are age 75 or older.