Large-Scale Review Identifies Pathways Linking Diabetes and Alzheimer’s Disease

Large-Scale Review Identifies Pathways Linking Diabetes and Alzheimer’s Disease

Melissa A. Schilling, a strategy and innovation expert at the NYU Stern School of Business, conducted a large-scale literature review of published studies on the association between diabetes and Alzheimer’s disease. Despite conflicting reports, Schilling was able to find evidence linking insulin, insulin-degrading enzyme (IDE), and Alzheimer’s, suggesting that avoiding excess insulin, while supporting IDE robust levels, might be key approaches to prevent and lessen the impact of Alzheimer’s disease.

The research article, which summarizes contradictions in this area of research and details future implications in policy and future study opportunities, is titled “Unraveling Alzheimer’s: Making Sense of the Relationship between Diabetes and Alzheimer’s Disease,” and was published in the Journal of Alzheimer’s Disease.

Alzheimer’s disease, a condition that affects millions worldwide, is currently treated with drugs that ameliorate symptoms and provide some relief to the patient, but they do not treat the cause of the disease. According to the Alzheimer’s Association, if a more effective treatment is not discovered, the disease may cost the United States $1.1 trillion per year by 2050, with expenses mostly going to nursing home care and home care, with up to 16 million American people affected.

Hopes of finding a cure have been hindered by the abundance of research that seems to contradict itself. The connection between type 2 diabetes mellitus (T2DM) and Alzheimer’s is a prime example of such incongruences. While some studies point to insulin deficiency as a primary cause, suggesting a benefit in inhibiting IDE, others conclude that hyperinsulinemia is to blame.

According to Schilling’s conclusions, there is indeed a relationship between insulin, IDE, and Alzheimer’s that yields multiple pathways to the disease depending on where the defect occurs. In a normal situation, insulin upregulates the expression of IDE, which subsequently breaks insulin down, leading to its decreased levels. Research has shown that IDE also plays important roles in breaking down Aβ, whose accumulation is one of the major hallmarks of Alzheimer’s disease.

Schilling found evidence of at least four different ways this cycle can malfunction and lead to Alzheimer’s. Identification of such malfunctions is important as the specific mechanism by which the disease arises strongly determines what treatments are likely to be effective. For example, if insulin deficiency is the main cause, intranasal insulin might benefit the patient. On the other hand, if hyperinsulinemia is the cause, then administering intranasal insulin could exacerbate the disease.

Schilling suggested there is enough evidence indicating that testing for glucose tolerance should occur early and often and, as obesity is also strongly associated with hyperinsulinemia and diabetes, glucose intolerance testing should become a standard part of regular health screening. This is especially important as diabetes is still fairly undiagnosed in the U.S. and many more people are pre-diabetic.

Early identification of diabetes and pre-diabetes, for example by testing hemoglobin A1c levels, could significantly lessen the impact of both diabetes and, possibly, Alzheimer’s.

According to Schilling, her findings strongly recommend policy changes, namely the identification of glycemic index on food products.

“What I’ve learned from my innovation research is that specialists can become trapped in the logic of their field, so new perspectives often come from outsiders,” Schilling said in an NYU press release. “If we can raise awareness and get more people tested for hyperinsulinemia, especially those who have been diagnosed with or who are at risk for dementia, it could significantly lessen the incidence of Alzheimer’s disease and vascular dementia, as well as other diabetes-related health problems.”

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