Authors: Suzanne M. de la Monte, M.D., M.P.H.1,2,3 and Jack R. Wands, M.D.3
Full Research Paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
Research Paper Summary:
In their paper “Alzheimer’s Disease Is Type 3 Diabetes–Evidence Reviewed,” Suzanne M. de la Monte and Jack R. Wands review human studies that provide evidence for the link between diabetes and Alzheimer’s disease. The scientist proposes a new perspective on the link between diabetes and Alzheimer’s disease. The authors suggest that Alzheimer’s disease may be a form of diabetes, specifically a “type 3” diabetes, characterized by insulin resistance and insulin deficiency in the brain. The paper reviews evidence from animal studies, human studies, and clinical trials to support this hypothesis. The authors argue that the similarities between Alzheimer’s disease and diabetes, including impaired glucose metabolism and inflammation, suggest a common underlying mechanism. The paper concludes by suggesting that targeting insulin resistance and other metabolic abnormalities in the brain may be a potential approach for preventing and treating Alzheimer’s disease.
One study that they discuss is a longitudinal study of 2,269 elderly participants in Rotterdam, Netherlands. The study found that individuals with type 2 diabetes had a significantly increased risk of developing Alzheimer’s disease compared to those without diabetes. Additionally, higher fasting glucose levels were associated with a greater risk of developing Alzheimer’s disease.
Another study they mention is a cross-sectional study of 47 cognitively normal adults in Rhode Island, USA. The study found that individuals with insulin resistance, as measured by the homeostatic model assessment of insulin resistance (HOMA-IR), had lower glucose metabolism in the brain as measured by positron emission tomography (PET). This suggests that insulin resistance in the brain may be associated with reduced brain function.
A third study they review is a randomized controlled trial of 104 elderly individuals with mild cognitive impairment (MCI) in Australia. The study found that a six-month intervention with a low glycemic index diet and physical activity led to improved cognitive function compared to a control group. This suggests that improving glucose metabolism and insulin sensitivity may have cognitive benefits.
Overall, these human studies support the hypothesis that there is a link between diabetes and Alzheimer’s disease, and that insulin resistance and impaired glucose metabolism in the brain may contribute to cognitive decline. These findings suggest that targeting metabolic abnormalities in the brain may be a promising approach for preventing and treating Alzheimer’s disease.
In conclusion, the evidence reviewed in this paper suggests that Alzheimer’s disease may be a form of diabetes, specifically a “type 3” diabetes, characterized by insulin resistance and insulin deficiency in the brain. The similarities between Alzheimer’s disease and diabetes, including impaired glucose metabolism and inflammation, suggest a common underlying mechanism. Targeting insulin resistance and other metabolic abnormalities in the brain may be a potential approach for preventing and treating Alzheimer’s disease. While more research is needed to fully understand the link between diabetes and Alzheimer’s disease, these findings have significant implications for the prevention and treatment of cognitive decline and dementia. Further studies exploring the potential of interventions targeting metabolic dysfunction in the brain are warranted, and may lead to the development of novel therapeutic strategies for Alzheimer’s disease.
