A new study explores the connections on a molecular level between Alzheimer’s and Type 2 diabetes, supporting the notion of Alzheimer’s as “Type 3 diabetes.”
The research found that a diet high in fat suppresses an essential gut protein, Jak3, which leads to Alzheimer’s-like changes in the brain in mice. It emphasizes the importance of managing diabetes and avoiding it through diet to reduce the risk of Alzheimer’s Disease.
The discoveries illuminate a possible path from diet through gut inflammation to brain health, offering hope for preventative strategies.
Findings suggest it should be possible to reduce the risk of Alzheimer’s Disease by keeping diabetes under control or avoiding it altogether, according to the research.
The study was led by an associate professor at Texas A&M University in College Station, Narendra Kumar.
“We think that diabetes and Alzheimer’s disease are strongly linked,” said Kumar, “and by taking preventative or amelioration measures for diabetes, we can prevent or at least significantly slow down the progression of the symptoms of dementia in Alzheimer’s disease.”
Kumar will present the new research at Discover BMB, the annual meeting of the American Society for Biochemistry and Molecular Biology, which will be held in San Antonio this month.
Alzheimer’s and diabetes are two of the most rapidly growing health concerns internationally. Diabetes alters the ability of the body to turn food into energy and affects an estimated 1 in 10 adults in the U.S.
Alzheimer’s is a form of dementia that causes a progressive decline in thinking skills and memory and is among one of the top 10 leading causes of death in the U.S.
Diet is known to influence the severity of diabetes’ health impacts as well as its severity. To discover how diet could affect Alzheimer’s development in individuals with diabetes, the researchers traced how a specific protein in the gut influences the brain.
They discovered a diet high in fat suppresses the expression of the protein Jak3 and that mice that don’t have this protein experienced a waterfall of inflammation beginning with the intestine, moving through the liver, and then on to the brain.
The mice ultimately showed signs of Alzheimer’s-like symptoms in the brain, including an overexpressed hyperphosphorylated tau and mouse beta-amyloid, along with evidence of cognitive impairment.
“Liver being the metabolizer for everything we eat, we think that the path from the gut to the brain goes through the liver,” said Kumar.
Kumar added that Kumar’s lab has been studying Jak3 functions for a long time, and they now know that changes in the Jak3 expression lead to a leaky gut. In turn, this results in diabetes, low-grade chronic inflammation, dementia-like symptoms, and a decreased ability of the brain to clear its toxic substances, as seen in Alzheimer’s disease.
According to Kumar, the good news is that this inflammatory pathway can be stopped by getting blood sugar under control as soon as possible and eating a healthy diet.
People with diabetes, in particular — which includes approximately 98 million adults in the U.S. — could benefit from adopting lifestyle changes to prevent the progression to Type 2 diabetes, reverse diabetes, and possibly reduce the risk of Alzheimer’s.
Critical facts:
• Preventative Potential: Avoiding or controlling diabetes through the management of blood sugar and diet could significantly reduce the risk of the development of Alzheimer’s disease.
• Molecular Connection: The suppression of the protein Jak3 in the gut because of a high-fat diet can initiate a cascade of inflammation that leads to the brain’s Alzheimer’s-like symptoms.
• Wide implications: With the vast number of adults in the U.S. with prediabetes, lifestyle changes to prevent diabetes might also mitigate the risk of Alzheimer’s, highlighting the intersection of neurodegeneration, diet, and metabolic health.
