For some years a faction of researchers have argued that Alzheimer's disease really should be considered a type 3 diabetes, based on the shared risk factors and what is known of the way that it ties into the mechanisms associated with insulin resistance. It is certainly the case that based on epidemiological data Alzheimer's, like type 2 diabetes, is enough of a lifestyle disease that you should add it to the list of very good reasons not let yourself become fat and sedentary. But is the connection with insulin metabolism relevant enough to class Alzheimer's as a form of diabetes, or is this just a good example of the way in which everything connects to everything else in the operation of our cellular biology?
Aging is known to be one of the top risk factors for both Alzheimer's disease (AD) and Type 2 Diabetes (T2D). The pathologies of these disorders are somewhat understood, with AD being associated with the accumulations of amyloid-β plaques and/or phosphorylated tau tangles (two proteins involved in neuron structure and development) and T2D being associated with resistance to insulin (the growth factor that controls glucose uptake by cells). For many years these two diseases have been treated separately, with few overlaps. In more recent years, however, the overlap between them has become more prominently recognized. The rate of AD in diabetic individuals is elevated, and it may be worth considering these two "separate" disorders as a related problem.
The first suggestion of AD being a previously unrecognized type of diabetes was in 2005, where it was noted that insulin signaling and insulin-like growth factor (IGF) expression were greatly affected in the instance of AD. It has since been shown that in the instance of AD, IGF, insulin receptor, and insulin expression are all reduced in the temporal cortex and hippocampus of the brain. Further, as AD progresses the levels of these gene transcripts continue to decrease. These inhibited insulin-related signals result in a deficiency and similar symptoms to those shown in other cases of diabetes. This deficiency also contributes to a vicious cycle, as impaired insulin receptor expression can contribute to further AD-like pathology such as hyperphosphorylation of tau and increased amyloid-β deposits as well as decreased clearance of these deposits from the brain.
Although seldom considered a metabolic disorder, it is clear that AD is metabolically affected in a similar fashion to diabetes. Although frequently treated separately, the same basic principles which are used for diagnosing an individual as diabetic may also be applied to understand some of the mechanisms affected in AD. As such, it may be appropriate to consider AD as a type of diabetes of the brain.