The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
And that's because we know that-- again, a common finding in patients with Alzheimer's disease is this glucose hypometabolism, some people are attributing it to insulin signaling impairment. And so some people are calling it type III diabetes. At the end of the day, I think the clearest signal that we have is that cells aren't getting enough energy from glucose as a fuel source.
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we now know that insulin is important for the processing of glucose in the brain the brain is very hungry for sugar you know and so any disruption in the brain's ability to to use glucose and to and to generate ATP from glucose is going to cause problems and this is a big thing in Alzheimer's disease glucose hypometabolism is one of the it's another one of the hallmark features in fact it's a feature that that by decades proceeds amyloid or tau aggregation
so that's why Alzheimer's disease has sometimes been called type 3 diabetes because what is your risk dramatically increases if you have type 2 diabetes or metabolic syndrome and there is some brain level insulin resistance
Alzheimer's has been called type 3 diabetes whatever right it's been said and there's plenty of literature about brain insulin resistance in Alzheimer's
A hallmark characteristic of Alzheimer's disease is glucose hypom metabolism.
I sort of view Alzheimer's disease as brain diabetes, and I think if the ApoE genotype as basically just a susceptibility. So I think anybody can get Alzheimer's disease with any genotype if there's enough insulin resistance, if there's basically enough difficulty in getting glucose through pyruvate dehydrogenase and into the Krebs cycle.