I think it's immoral and unkind to report on a medical trial and not be clear that it was in mice rather than humans.
Copper transport drug restores memory and clears toxic Alzheimer's proteins
81–90 of 150 posts
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#82My mother has early onset alzheimer's disease. We currently know very little about the disease and the current treatment options are controversial. The efficacy of the medications removing the amyloid plaque from the brain is questionable, as people still decline. What makes alzheimer's difficult is that it is not really a single uniform disease. There are subtypes. Since my mother has it, I was presented with an opt…
Give her -- and yourself -- lithium orotate. It's an asymmetric bet: it won't hurt, but very well might help. It has been found to be effective in murine models.
Yes see Dr Nehls for this.
and keto, beginning with MCT oil
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#83Lithium, too! In mice. https://otd.harvard.edu/news/could-lithium-explain-and-treat...
Interestingly, lithium does seem to protect telomeres and in fact lengthens them, which may affect Alzheimer's.
interesting, I remember reading population of Beijing seem to have lithium in their water or air so their new born and mothers carrying seem to have 20x of lithium concentration of what's considered normal...
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#84My mother has early onset alzheimer's disease. We currently know very little about the disease and the current treatment options are controversial. The efficacy of the medications removing the amyloid plaque from the brain is questionable, as people still decline. What makes alzheimer's difficult is that it is not really a single uniform disease. There are subtypes. Since my mother has it, I was presented with an opt…
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Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#85Earlier quoted context omitted.
It is a repeating trend in all medical research. However enough does turn out to work in humans that we eventually make useful progress.
In general, sure, but in this specific instance (treating Alzheimer's by clearing amyloid-beta) it's been shown over and over again to not work in humans.
I’m kinda new to this - so what you’re saying is the mouse model induces beta-amyliods directly, rather than finding ways to give mice Alzheimer’s, whereas the human tests are for humans that have Alzheimer’s? Meaning we aren’t doing any tests of simply stimulating BA growth in humans?
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#86Earlier quoted context omitted.
AFAIK the background is the 'big 5' universities in Australia have a fat loan due which they took out 10 years ago and can't pay. Their primary income source was foreign exchange students and that demand has fallen off a cliff. So they're shedding academics and puffing like crazy right now. It seems in the near future Australian tertiary education will be highly corporatized and move to a more American model than our…
> foreign students FTFY. Not exchange students.
Erp, well caught.
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#87Earlier quoted context omitted.
> Over 56 days, the treatment reduced toxic amyloid-beta by 42 per cent and improved spatial learning by nearly 44 per cent So there's some benefit. Sounds like their next step is a much larger trial to answer the question you are posing.
The word "benefit" does not apply here. The only "benefits" patients and families care about are: 1) does the patient live longer, and/or 2) does the quality of life improve in a meaningful way? Amyloid plaques are a surrogate marker, and (as already explained by many people in this thread) have not been established as a causal factor in disease. In fact, some work has even suggested a protective role for plaques. So…
> improved spatial learning by nearly 44 per cent
We care about this part
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#88Earlier quoted context omitted.
It is a repeating trend in all medical research. However enough does turn out to work in humans that we eventually make useful progress.
In general, sure, but in this specific instance (treating Alzheimer's by clearing amyloid-beta) it's been shown over and over again to not work in humans.
Which is not the point of the research paper: the point of it is they've targeted a novel mechanism (waste clearing) and observed two effects impacting markers for Alzheimer's.
Amyloid beta might not be causative, but if you hit a mechanism then it stands to reason it might be indicative - in this case if Alzheimer's is partly or fully caused by a waste removal problem in the brain.
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#89Alzheimer’s is driven by the buildup of toxic proteins called amyloid-beta. In the words of Derek Lowe: Amyloid-directed therapies truly, truly do not appear to be the answer for Alzheimer’s treatment. When I started work in the field back in the early 1990s, I was convinced of the opposite - the evidence looked very strong that defects in amyloid processing were indeed the cause of the disease. But that was thirty-f…
Having said that, this therapy could be improving clearing of all sorts of things, not just amyloid-beta. If amyloid is just a misleading side effect, clearing it could also be misleading.
Re: Copper transport drug restores memory and clears toxic Alzheimer's proteins
#90Earlier quoted context omitted.
In general, sure, but in this specific instance (treating Alzheimer's by clearing amyloid-beta) it's been shown over and over again to not work in humans.
I’m kinda new to this - so what you’re saying is the mouse model induces beta-amyliods directly, rather than finding ways to give mice Alzheimer’s, whereas the human tests are for humans that have Alzheimer’s? Meaning we aren’t doing any tests of simply stimulating BA growth in humans?
I'm also not exactly on expert on this myself, take it with a grain of salt, but my understanding is that we don't really know what Alzheimer's is. To our knowledge there isn't a clear physical cause we can point to - a virus or bacteria or tumor or something. We have the symptoms, and we have the observation that Alzheimer's patients have amyloid plaques in their brain - among other differences!
Since mice don't ever get Alzheimer's naturally, and we don't actually know what Alzheimer's is, we don't know what it would even mean to give mice Alzheimer's. But for research we've genetically engineered mice that end up with lots of those plaques, and their behaviour does suggest an impairment similar to Alzheimer's, so that's what we've been working with. And in those models, various treatments that involve clearing the plaques does seem to help resolve that impairment - but they don't help humans with Alzheimer's, even if they do clear the plaques there too.
If I'm reading your question correctly, we can't stimulate amyloid plaque growth in humans for experimentation because that'd almost certainly be considered completely unethical. And also our methods for inducing the amyloid plaques involve mice that are genetically modified from birth rather than something we introduce in vivo, which would somehow be even more unethical than experimenting on live humans. It's possible we could make those genetic modifications in vivo now with recent developments in gene therapy, but...why?