Alzheimer’s disease certainly has an inflammatory component to it, as do other neurodegenerative conditions. The immune system of the brain runs awry in characteristic ways. Evidence exists to suggest that short-lived advanced glycation end products (AGEs) of the sort found in individuals with metabolic syndrome and type 2 diabetes are a significant source of inflammation. They act via the receptor for AGEs, RAGE. This, I should note, is entirely unrelated to the detrimental effects of persistent, long-lived AGEs on tissue structure. Short-lived AGEs are more of a lifestyle issue, in that everyone has them to some degree, but they are strongly associated with diet, obesity, and the metabolic diseases of obesity.
In any case, some effort has gone into building ways to interfere in RAGE-induced inflammation, and one of them made it as far as clinical trials for Alzheimer’s disease. Unfortunately it joins the sizable and growing pyre of failed trials for this condition – and by the look of it was running largely on hope for much of its lifetime, one of many things wrong with the present system of trials and its dominant focus on
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