Some researchers believe the connection between impaired glucose metabolism, insulin signaling and AD is so strong that they refer to AD as “type 3 diabetes.” In fact, type 2 diabetes (T2D)—a condition stemming from broken glucose metabolism and insulin signaling—has been identified as an additional risk factor for developing AD. Moreover, the pathological changes that occur in AD in the brain physically resemble those seen in the pancreas and vasculature in T2D. Type 2 diabetics who carry ApoE4 alleles are at the greatest risk for AD, with an even more severe risk reserved for those treated with exogenous insulin.19 This suggests that either T2D or related features of the metabolic syndrome bring about AD, or that they are separate consequences of the same underlying cause—and moreover, that insulin is a key factor.
That not all type 2 diabetics develop AD and not all AD patients are diabetic should disabuse us of the notion that diabetes causes AD. What is more likely—and what the research seems to support—is that they are physiological cousins. That is, they result from the same underlying metabolic imbalances, but manifest differently depending on which parts of the body are affected.