CBDA THCA Alzheimer’s

are you talking about HU-211 or GAT211?

1 Like

Gat 211…glad to see you picked up like that.
The PAM effect of GAT 211: think of it as altering the radar plot, more than just an increase in THC action.

A brief review of GPCR bias and representation a “radar”plots: Receptors | Free Full-Text | Biased Agonism or “Biaism” for Dummies: A Commentary

Cut and paste

1 Like

Gat 211

1 Like

Just a thought…I know CBD has been shown to reduce insulin resistance significantly. I also have been reading about type 3-4 diabetes which many believe to be the underlying cause of alzheimer and dementia. Maybe there is a causal link between the CBD and insulin resistance and battling alzheimers.


Sure – and i’d say, maybe you might want to do that for like 6 months – 1 week is crazy small when you’re talking about breaking down what’s become a substantial portion of their brain mass…

I should also point out just “removing plaques” isn’t really as good as it sounds. Cause it’s not like when you remove plaque suddenly there’s healthy tissue in it’s place. No, you’re just left with a big honking hole. That’s why these recent amyloid antibodies like aduhelm all reduce total brain volume. The idea that removing plaque actually will improve cognitive function in my view is totally unproven… the most I would expect is that it could slow further progression but not actually undo any damage already done, and even that does not actually have hard data supporting it. Hell, it could make things worse if it leads to some kind of regional structural collapses…

By the time you’ve got so much plaque that your brain volume drops 10% when it’s removed, your brain is freaking swiss cheese. I don’t see any sort of medications fixing that one, not in 100 years. What we need is a handle on the actual causative factors and treat it preventatively. Nothing i’ve seen convinces me “curing” or “reversing” alzheimers is a realistic goal. Something is fundamentally wrong with the mouse models that every lever that changes their outcome, generates null results in humans. The mouse models simply mutate them to secrete more beta-amyloid. Seems like the human disease has causative factors going at least one step deeper than that that keep on trucking no matter what you do to the amyloid production process.


I absolutely see your logic here, my only counter is how miraculous the human brain is. Have you heard of the gentleman who had 90% of his brain mass missing and still lead a completely normal life? The brain has been shown to do amazing things in the wake of extreme trauma.


6 months …if you really think you can reverse plaque formation? How about rapid cognitive improvement? You can observe such improvements using cholinergic agonists.
Cognitive capabilities are emergent phenomenon. None regard such actions a “curative” in an manner.

Yes “ Rescue Memory Deficits and Reduce Amyloid-Beta and Tau”. Is a very shocking claim! Certainly, your criticisms if the topic/field are needed. I have not read the paper in sufficient detail to offer any specific critique of their experimental design or interpretation of results. Just mostly interested in the CBDA/THCA protocols. Which if my memory serves me seemed high 1-10 micromolar using Tween?

The Wnt signaling pathway most interesting .

There is anecdotal evidence that CBDA/cbd can interact with these signaling pathways.

You might also look closely at the History of “humanized mice” as a tool in preclinical studies. Try wikipedia for a start. A lot has changed over the past “50 years”…
It sort of explains why there are 100s of mouse models.


1 Like

I have heard about that and I confess I don’t have any explanation for it. But if anything, it seems like it just casts further doubt on plaques being the real causative factor, since they don’t disrupt nearly the brain volume that man’s hydrocephalous did. There was a similar case involving someone born with little more than a brain stem but at least managed to live (though I think in that case they were completely disabled).

At any rate, this point should be clear – we have drugs that effectively remove plaque in humans now but still don’t affect cognitive decline. These same drugs also remove plaque in the best mouse models and do affect cognitive decline. So we can’t consider either plaque removal or reversal of cognitive decline in mice, to be valid proxies for it working in humans. Only true human trials can do that, and ones that test cognition DIRECTLY, not act like “amount of plaque removed” can be used as a proxy endpoint. It was essentially that last point, by the way, that led the FDA’s advisory board to resign over adulhelm’s approval. Plenty of amyloid reduction but nothing when it comes to actually helping people.

1 Like

“Making sure everyone is on same page when it comes to “amyloid proteins”.

Deposits of aggregates of particular proteins are specific hallmarks of a wide range of neurodegenerative diseases [1]. Aggregates of misfolded proteins with altered degradation can be located intracellularly and/or extracellularly. The most important primary intracellular proteins include:*

  1. Hyperphosphorylated protein tau in Alzheimer’s disease (AD) [2], tauopathies including frontotemporal lobar degenerations with tau pathology (FTLD-tau) [3];

  2. Alpha-synuclein in Lewy bodies in Parkinson disease (PD) and dementia with cortical Lewy bodies (DLB) or in oligodendroglial inclusions in multiple systemic atrophy (MSA);

  3. Phosphorylated TDP-43 in frontotemporal lobar degeneration with TDP-43-positive inclusions (FTLD-TDP) [4];

  4. Ubiquitin in frontotemporal lobar degeneration with inclusions positive for ubiquitin-proteasome system markers (FTLD-UPS) [4,5];

  5. Fused in sarcoma (FUS) inclusions in FTDL-FUS [6].

Primary extracellular protein aggregates, in optical microscopy called “plaques,” can be observed in cortical locations in:

  1. AD [7];

  2. Prion diseases (Creutzfeldt–Jakob disease (CJD), Gerstmann–Sträussler–Scheinker syndrome (GSS), fatal familial insomnia (FFI), and kuru) [8].

IJMS | Free Full-Text | Extracellular Amyloid Deposits in Alzheimer’s and Creutzfeldt–Jakob Disease: Similar Behavior of Different Proteins?

The frontal temporal stuff is the hardest on the families. I have read that the afflicted cycle through 2-3 entirely different personalities all of which none can put up with…
So it is all not just losing your marbles. The Parkinson’s and MSA conditions…are somewhat worse…the aspects of latter include loss of autonomic functions…like wide awake and experiencing your own decrepitude…and fully aware …
Everyone has so much to look forward to …
Dealing with an elder family member who has passed through such states leaves a lasting impression. There is something to say about “live fast, die young and have a beautiful corpse”…

‘’BTW”. One of those hydrocephalus men in England taught math at a local community college…something like that.

1 Like