Neuroinflammation, Type 2 diabetes, and dementia

Neuroinflammation is a strong candidate to explain, at least in part, the increased dementia risk in type 2 diabetes (T2D). Currently, this hypothesis is largely circumstantial, based on clinical and experimental findings indicating that neuroinflammation has a more important role in the pathogenesis of neurodegenerative disorders including Alzheimer's disease (AD) than previously considered and evidence that T2D is a disorder with a strong inflammatory component that may promote neuroinflammation. A number of animal models have been studied that indicate that T2D or related pathophysiological processes are able to exacerbate AD-related processes via inflammatory pathways. Advances in positron emission tomography with radioligands that quantify neuroinflammation provide an opportunity to study whether chronic peripheral inflammatory states seen in T2D lead to increased neuroinflammation and contribute to cognitive decline in this common age-related condition.