Scientists Develop Potentially Vital Nasal Vaccine For Treating Alzheimer's 36
Researchers have developed a nasal Alzheimer's vaccine that was successful in reducing atrophied brain matter in mice by blocking a protein that causes the disease. It also reduced changes and abnormal behavior in the brain normally associated with the disease. The study was published in the journal Nature. Interesting Engineering reports: "Much more research is necessary for the vaccine to be used in humans, but it is an accomplishment that can contribute to the development of a dementia cure," team member Haruhisa Inoue, a professor at Kyoto University, told The Asahi Shimbun. Alzheimer's disease and other forms of dementia are characterized by an abnormal accumulation of tau proteins in the brain. In the study, the research team incorporated a gene into a harmless virus to make it produce tau.
They then administered the virus nasally to mice with genes that made them prone to developing dementia. The vaccine proceeded to stimulate the mice's immune system, causing them to build antibodies that removed the tau proteins. These antibodies were more than double in mice who had the vaccine administered compared to those that did not. In addition, the vaccinated mice's brain areas were only two-thirds as atrophied as those who were not vaccinated. Finally, no detrimental side effects were recorded during the eight months the scientists observed the mice.
They then administered the virus nasally to mice with genes that made them prone to developing dementia. The vaccine proceeded to stimulate the mice's immune system, causing them to build antibodies that removed the tau proteins. These antibodies were more than double in mice who had the vaccine administered compared to those that did not. In addition, the vaccinated mice's brain areas were only two-thirds as atrophied as those who were not vaccinated. Finally, no detrimental side effects were recorded during the eight months the scientists observed the mice.
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Perhaps it works by using the pathways that the nerves in the sinus cavity follow, in order to more directly reach the brain where it's needed?
The sinus cavities and the eyes have been implicated in the past as vectors for infection of the brain.
Headlines, important words first please. (Score:2)
Re:Headlines, important words first please. (Score:5, Insightful)
Well, the really important words that need to be in that title (and the title of the article):
IN MICE
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Let's test it on Joe Biden. I have sympathy for the mice.
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Let's test it on Joe Biden.
Anybody else noticing his pupils turning more and more black?
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The required caveat is already in the title: "potentially".
But in fairness, do you know how similar the immunoresponse system of humans and mice are? There is objectively enough reason to have some hope here.
Re:Headlines, important words first please. (Score:5, Interesting)
I saw a quote from a scientist in this field a few years back (they had discovered that putting mice once a day for an hour in a room with LEDs that flashed at a particular frequency led to a near total reduction in the plaque associated with Alzheimer’s and a near total restoration of their cognitive functions). They were asked whether they were hopeful a human treatment would arrive soon based on their work. They quickly pointed out that in other fields, a successful treatment in mice apparently translates to promising results in humans with a very high rate (60+%? I don’t recall the exact number). In contrast, the rate at which successful treatments in mice in the area of neuroscience translate to successful treatments in humans is less than 2%.
All of which is to say, there have been promising results for years in mice with regards to Alzheimer’s, but very few have translated to anything actionable in humans. Have hope, but don’t bank on it.
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Re:Headlines, important words first please. (Score:4, Informative)
Obviously, take this with a MASSIVE grain of salt since my area of expertise (software) is wholly unrelated and my recollection is admittedly hazy at this point, but I think the article I read began with the scientists observing that brainwaves operated at different frequencies when engaging in different processes. During the nightly cleaning process that removes plaque in brains of healthy individuals, brainwaves were measured at X (a number I don't remember at this point), but in individuals with Alzheimer's the brain did not engage in cleaning nor did the brainwaves they measured operate at that same frequency. The scientists wanted to test whether it was possible to trigger the cleaning process if they could induce the brain to operate at X frequency.
From what I recall in the article, nerve cells or neurons (or something...again, I'm hazy since it's been a few years) react/are receptive to light, so the scientists began by surgically implanting a fiber optic line or lines directly into the brains of these mice. After trying out a number of different frequencies for their pulses of light, they were able to see that the brain did indeed react and that they were able to induce different states. Specifically, when pulsing light at—I believe—60 Hz, they saw that the brainwaves matched the X frequency that they expected in a healthy individual, and memory tests indicated significantly improved recollection among those mice, at least on a temporary basis.
Subsequently, they wanted to see if they could bypass the fiber optic line and instead use the optic nerve as a conduit for those pulses. After a bit of engineering, they were eventually able to construct a room with banks of LED lights pulsing at 60 Hz that would do the trick. Merely leaving the mouse in the room for an hour would trigger the cleaning process, buying the mouse about a day of full recollection before a gradual decline to their previous state of poor recollection. Still later, they were able to simplify it from a room to a simple, horizontal box of LEDs.
(EDIT right before I submit: I did a quick search [google.com] just to see if I could find the original article I read, and while I don't see it, nor do I see anyone mentioning the specific claim I originally made about the low degree of usefulness between research in mice neuroscience and applications in humans, there are quite a few write ups regarding the research I was talking about. In quickly skimming through one or two, it looks like I got a few minor facts wrong (40 Hz, not 60 Hz; last year, not a few years ago). I left my original post intact with those errors (and likely more) since I didn't want to pretend that I remembered those details correctly, so I'd encourage you to read through some of those articles if you're interested in the topic.)
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Sorry to double-post, but right after I submitted, I noticed this research paper that gets into the specific mechanism you were asking about:
https://www.ncbi.nlm.nih.gov/p... [nih.gov]
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The mouse Alzheimer's models are very different from the human one. To be fair, nobody knows how the human Alzheimer's disease works. They know doing certain things to mice create an effect that is somewhat similar. Doing those things to the mice and then trying to fix them isn't a good model for fixing those things in people, so so far every attempt to transfer working results between mice in people in this area has failed. That doesn't mean the next one will, but it sure isn't encouraging.
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"E.g. Alzheimer's treatment, potential vaccine, nasal."
Vaccine gives you only 2 thirds Alzheimer, yeah.
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2/3rds heart disease would be wonderful. 2/3rds cancer would be, etc.
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Bloody important stuff (Score:3)
The lack of interest in this article is a bit disconcerting because if you would ask me what the major issues would be which scientists should work on , Alzheimers would be at the top. And this scientific advance looks promising. Maybe people don't post on it not because the article isn't worthwhile but because they can find of nothing interesting to say. Which is fine I guess.
Re: Bloody important stuff (Score:3)
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But the mouse models for Alzheimer's disease appear to be terrible. Not just mildly bad. Perhaps they should create hamster models.
Of course, my real suspicion is that they totally misunderstand what's going on, and that's why the models they create don't work. But what's certain is that the mouse models they've used so far don't work.
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I'm not even sure that other primates, even chimpanzees, would be a good model, but it might be. However if they must induce the failure mode, then the model will only be as good as their theory about the disease. And current evidence is that we don't have an even approximately adequate theory of the disease. If we did, we could probably implement it in a mouse model.
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I don't have the background to be able to judge mice studies but it's a good warning.
I'm tempted to believe it's magnitudes better than in vitro AND in this case they have a realistic method for administering the medicine (for the medicine to reach its target), but yeah I need to sample some of these histories to get a feel of the many reasons why a study fails at a later stage.
The main reason why a lot of studies fail would be that in our PR society they are released to the public much too soon...
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Nothing horrifies me more than the thought of losing control of one's own mind, and with Alzheimers you're aware of what's happening and that you have absolutely no control which is even more awful. By all the gods above, below and nonexistent I would immediately take up cliff climbing or something equally dangerous.
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Seems like that's on you for conflating controversy, importance, and interest, as you even alluded to.
Maybe we should add a "like" button to Slashdot so that we can show we like it, so you aren't put out.
Oh, joy (Score:4, Funny)
In the study, the research team incorporated a gene into a harmless virus to make it produce tau.
This wouldn't be in a Chinese lab that by total coincidence is 7km from some huge dementia outbreak, would it?
A vaccine? Did I miss something? (Score:1)
Well it fixes the defect they introduced (Score:1)