Abstract
Background: Diabetes is considered as a risk factor for Alzheimer’s Disease, but it is yet unclear whether this pathological link is reciprocal. Although Alzheimer’s disease and diabetes appear as entirely different pathological entities affecting the Central Nervous System and a peripheral organ (pancreas), respectively, they share a common pathological core. Recent evidence suggests that in the pancreas in the case of diabetes, as in the brain for Alzheimer’s Disease, the initial pathological event may be the accumulation of toxic proteins yielding amyloidosis. Moreover, in both pathologies, amyloidosis is likely responsible for local inflammation, which acts as a driving force for cell death and tissue degeneration. These pathological events are all inter-connected and establish a vicious cycle resulting in the progressive character of both pathologies.
Objective: To address the literature supporting the hypothesis of a common pathological core for both diseases.
Discussion: We will focus on the analogies and differences between the disease-related inflammatory changes in a peripheral organ, such as the pancreas, versus those observed in the brain. Recent evidence suggesting an impact of peripheral inflammation on neuroinflammation in Alzheimer’s disease will be presented.
Conclusion: We propose that it is now necessary to consider whether neuroinflammation in Alzheimer’s disease affects inflammation in the pancreas related to diabetes.
Keywords: Amyloidosis, insulin resistance, hyperglycemia, vasculopathy, innate immune response, microglia, cytokines, advanced glycation end products.
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