A recent study in mice suggests the the liver is key in a molecular link that may also cause humans with diabetes to develop Alzheimer’s disease.

Unlike type 1 diabetes, type 2 diabetes is overwhelmingly in obese people so if the findings in mice ever apply to humans the prevention of Alzheimer’s disease in such people could be avoiding it in the first place.

Alzheimer’s is a poorly understood dementia with little meaningful progress this century, while type 2 diabetes has become more common as wealthy countries have so much affordable food even the poorest residents can be fat. In type 2 diabetes, the body becomes over-taxed by processing food and people develop an inability to easily to turn food into energy. It is often prevented by maintaining healthy white and sometimes treated with weight loss but it currently  affects up to 1 in 10 U.S. adults. 

To create a link between diet in people with type 2 diabetes and the development of Alzheimer’s, the researchers traced how a particular protein in the gut may influence the brain in mice. In their test mice, they found that a high-fat diet suppresses the expression of the protein Jak3 and that mice without this protein experienced a cascade of inflammation starting with the intestine, moving through the liver and on to the brain.

Ultimately, the mice showed signs of Alzheimer’s-like symptoms in the brain, including an overexpressed mouse beta-amyloid and hyperphosphorylated tau, as well as evidence of cognitive impairment. If it is relevant in humans it may be possible to stop this inflammatory pathway by eating a healthy diet and getting blood sugar under control as early as possible. They highlight that adults who are obese but not yet diabetic - the U.S. CDC is the only science body in the world that picked a blood a1c level and declared it 'prediabetes' and an epidemic affecting a third of the country - might prevent the progression to Type 2 diabetes and potentially reduce the risk of Alzheimer’s.

However, there is no plausible biological mechanism for how they could be related in humans, beyond obesity being a risk factor and co-morbidity in everything. For now the results are only EXPLORATORY. Mice are not little people.