This 2017 review examines the evidence linking Alzheimer’s disease to diabetes, insulin resistance, and broader metabolic dysfunction. The authors argue that Alzheimer’s shares several key features with type 2 diabetes, including impaired insulin signaling, mitochondrial dysfunction, oxidative stress, inflammation, advanced glycation end products, and disrupted glucose metabolism in the brain.

Insulin plays important roles in the brain, including glucose metabolism, synaptic plasticity, memory formation, amyloid-beta clearance, and tau regulation. When insulin signaling becomes impaired, the brain may become less able to use glucose efficiently, while amyloid-beta, tau phosphorylation, ROS production, mitochondrial damage, and inflammation increase. The review describes this as a possible basis for calling Alzheimer’s “type 3 diabetes.”

The evidence remains incomplete, but the metabolic pattern is hard to ignore: diabetes, hyperinsulinemia, and insulin resistance are repeatedly linked to higher Alzheimer’s risk, while cerebral glucose hypometabolism can appear decades before symptoms. The paper supports the idea that Alzheimer’s may not be only a disease of amyloid plaques, but also a disease of impaired brain energy metabolism.

https://www.sciencedirect.com/science/article/pii/S0925443916302150