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Abstract highlights:

• In recent years, more and more evidence has proved that insulin regulates various functions of the brain.
• The hippocampus, one of the earliest brain regions affected by AD, is widely distributed with insulin receptors.
  • Studies have shown that type 2 diabetes mellitus, characterized by insulin resistance, is closely related to AD, which has drawn extensive attention to the relationship between hippocampal insulin signaling and AD.
• We also highlight the molecular link between hippocampal insulin resistance and AD and provide a theoretical basis for finding new therapeutic targets for AD in clinical practice.
• As a common link between T2DM and AD, in recent years, insulin resistance has been shown to contribute directly or indirectly to the progression of AD.

Is it fair to assume that a low carb / low GI diet is a preventable measure against AD?

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Yes. Less sugar/artificial sugars/insulin spiking foods = less insulin = greatly lowered risk of insulin resistance = lowered risk of CNS insulin dysfunction and neurodegeneration = lower risk of AD. Insulin resistance causing widespread insulin dysfunction which eventually overrides the CNS's defenses and causes CNS insulin malfunction is what causes AD.

There is a fantastic diagram within the original article of the post depicting how peripheral insulin resistance seen in Type 2 diabetes progressively invades the CNS. (Figure 1)

Oh boy this is FASCINATING

Having your foods with carbs also have a high amount of fiber is probably more important than counting carbs

There seem to be hundreds of tantalizing leads about Alzheimers, all going in different directions.

I figure there are multiple ways to Alzheimer, but similarities to each one can help narrow down to one or few true causes. Maybe it isn't insulin itself, but whatever cell/system in the body insulin reacts to that causes Alzheimers. Or maybe a combination of insulin and other drugs/nutrients/etc that triggers some effect. Feels like a job for deep learning ai to find.

Also, some leads might not even be true leads after all.

Not for nothing do we sometimes refer to Alzheimer’s as “diabetes mellitus type 3.”

Precisely. I wanted to share this to help some people potentially become more open to the idea, since it is supported by “official” medical research

I’m still working my way through the paper, but I’ve read enough to think that my frequently expressed hypothesis that there is something fundamentally different about the brains of people with type 2 diabetes, something that seems to blunt their affective responses and lead to generalised apathy, is not so out there after all. You can see this blasé approach to life even in very young patients before they have an official diagnosis of type 2 diabetes. I work with them every single day, and I still find their impenetrable lack of passion for, well, anything just as disconcerting as the first time I encountered it. There has to be some sort of genetic mutation endemic to the type 2 diabetic population that accounts for this.

Do you know if there’s been any Alzheimer’s studies with medications that combat insulin resistance like metformin and GLP-1 agonists (semaglutide and tirzepatide)?

The book why I'm sick talks about this. Came out in 2020. Not the 1974 book also good.

I remember listening to a talk where apparently metaformin was being studied for anti aging potential since it seemed to reduce a range of diseases that occur with increased age like AD and cancers.

Blood vessels are the unifying thing. Most established risk factors for Alzheimer's relate to blood vessel health (hypertension, hyperlipidemia, diabetes, smoking), proxies for bad blood vessels (heart attacks, congestive heart failure, stroke, peripheral artery disease, kidney failure) and aging. Sure enough there is a thing that builds up in blood vessels as we age called medin that seems to be some kind of detritus from stuff that holds vascular cells together. And sure enough there is evidence that blood vessels with medin adjacent to brain lead to amyloid plaques/tangles we have been chasing for decades, but as others have called it, those plaques are the smoke, not the fire.

I suspect when you read about viruses/inflammation being linked to neurodegenerative processes, you're really just talking about leaking medin/other crap into the brain.

I believe an AI study concluded that the strongest risk factor for developing dementia was leaking proteins in the urine. Because proteins aren't supposed to be leaking from anywhere, so if they are leaking in the urine, then they are probably leaking in the brain.

And strongest risk factor for that kind of leaking? Diabetes.

If I were treating stocks like gambling, I would invest it all in any pharmaceutical company that is developing antibody to medin

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T2D folks who go low carb/keto reverse their diabetes. It's not genetic. (Or at least not in 99+% of people.) I'd postulate that what's causing T2D is causing mental aberrations.

That’s a peculiar argument to make in this context. Amenablity to lifestyle changes and inheritance are not mutually exclusive characteristics. It’s certainly true that diabetes can be slowed or reversed through dietary changes, but it’s also pretty well established that there is a strong genetic component to the disease. Similarly, the effects of PKU can be ameliorated through lifestyle changes, even though it’s most definitely a genetic condition.