5 ms·
Alzheimer's biomarkers now visible up to a decade ahead of symptoms
- 01-_- 2y agowell, now we have excellent news <3
- jimlawruk 2y ago> Catching these clumps early while still in minute quantities can enable effective intervention I wonder what interventions they mean here. Drugs, lifestyle changes?
- caycep 2y agoPresumably, a newer generation of anti-amyloid or anti tau agents. There are current gen ones (targeted monoclonal ab ) which aren’t that incredibly effective but there’s some thought that maybe that’s due to treating the wrong patients at the wrong time, vs starting therapy earlier on
- WillyWonkaJr 2y agoDidn't it turn out that the amyloid plaque hypothesis was based on a fraudulent paper?
- pedalpete 2y agoNot exactly. There are "issues" with one of the early papers, and I believe some other follow-up papers, but not all research had these issues.
- thaumasiotes 2y agoNothing. We don't know of an intervention for Alzheimer's. Early detection can enable effective intervention, but in this case it doesn't.
- snailmailstare 2y agoWe have a lot of correlations and theories and now we can test over more than 10 years and see what happens when with patients where we have successfully kept these markers down from a much earlier start. I just hope they control correctly for brain bleeds and premature death.
- thaumasiotes 2y agoThat will be a fun set of experiments. As far as I'm aware, we currently have no evidence to suggest whether the appropriate model for this protein accumulation is more "it's like a cancer growing on your organ" or "it's like a scab growing over an open wound". Are scabs markers of injury? Of course. Could we reduce injuries by preventing the development of scabs? No, that's a new horrifying medical condition called hemophilia. In the general case, it's rapidly fatal. This is something that really bothers me about the current craze for suppressing inflammation. In that case, we already know that inflammation is like scabs, a defensive reaction against some other problem. For Alzheimer's, we don't know anything.
- trashface 2y agoProbably not going to be super popular but maybe heating your brain for 20 years? https://text.npr.org/nx-s1-5293253 https://text.npr.org/nx-s1-5293253
- bondant 2y agoIf going to the sauna daily is all it takes to prevent it, that would be quite a thing!
- maest 2y agoIs Alzheimer's less prevalent in sauna going populatioo?
- bondant 2y agoI don't know, but the parent's link article says: >"I spent 20 years in the Navy, most of it in the hot spots, like the engine rooms of ships—110 degrees is nothing on a ship," he says. That environment may have caused an increase in heat shock proteins, which were able to limit the spread of tau and prevent the onset of Alzheimer's. The scientists studying Whitney aren't sure if that's all, or even part, of the explanation. But they are hoping that the paper on Whitney will encourage other researchers to look for answers. So instead of going to work for the navy, one could just go to the sauna daily. Edit: turns out that it might be true: https://academic.oup.com/ageing/article/46/2/245/2654230?login=false https://academic.oup.com/ageing/article/46/2/245/2654230?log...
- askonomm 2y agoAccording to this it would be the opposite: https://pubmed.ncbi.nlm.nih.gov/28687259/ https://pubmed.ncbi.nlm.nih.gov/28687259/ So maybe Sauna is good, but where Sauna is popular is usually a place that is very cold and humid, which is not good.
- memkit 2y agoFinland has huge toxic algae bloom problems. The link between BMAA (from toxic algae blooms) and neurodegenerative diseases in predisposed people is basically causal and proven at this point, but it's allegedly suppressed by Big Fishing and Aquaculture. You may be right. There are many other components contributing to the problem in Finland, too.
- josephpmay 2y agoThere’s been evidence recently that GLP-1 Agonists can delay the onset of Alzheimer's symptoms. Look up the evoke and evoke+ trials. This might be the first “real” treatment for Alzheimer’s, and it’s relatively low risk.
- nwienert 2y agoGLP-1 agonists are life extension drugs, they cure way more than just weight.
- pedalpete 2y agoWe've been developing Sleep slow-wave enhancement tech for the last few years, and studies are showing promise as a potential prevention and management of AD. These links were not using our tech, but are based on the same principles of phase-targeted slow-wave enhancement. We have an enhanced protocol aiming to overcome some of the issues these researchers experienced with previous implementations. https://pmc.ncbi.nlm.nih.gov/articles/PMC10758173/ https://pmc.ncbi.nlm.nih.gov/articles/PMC10758173/ https://jcsm.aasm.org/doi/10.5664/jcsm.10778 https://jcsm.aasm.org/doi/10.5664/jcsm.10778
- glaugh 2y ago> …small amounts of clumping tau protein in the brain and cerebrospinal fluid, which lead to Alzheimer's disease. I don’t think this should be stated as a proven fact anymore, given the doubt now cast over the amyloid hypothesis This is a nice summary of the case: https://podcasts.apple.com/us/podcast/plain-english-with-derek-thompson/id1594471023?i=1000691074414 https://podcasts.apple.com/us/podcast/plain-english-with-der...
- im3w1l 2y agoI've seen this point brought up many times over the years and yet research in this direction seems to continue, so I think there must be more to it. I asked chatgpt about it, and it claims that the controversial paper was influential but it was more about a certain sub-hypothesis that got called into question after that rather than the entire thing. Now I know that bringing up chatgpt is frowned upon here but I thought I should make an exception for this case as its not so easy for me to answer otherwise.
- robwwilliams 2y agoYou might enjoy “How Not To Study A Disease: The Story of Alzheimer’s” by Karl Herrup (2023, MIT Press). Great sad overview of the hegemony of the Abeta hypothesis that now has a Tau hypothesis buddy. https://mitpress.mit.edu/9780262546010/how-not-to-study-a-disease/ https://mitpress.mit.edu/9780262546010/how-not-to-study-a-di...
- robwwilliams 2y agoAgree strongly with you. This statement make Alzheimer’s into a wonderfully “simple” monogenic disease like Huntington’s but all age-related disease have many complex interwoven weaker and stronger causes—-even Huntington’s disease in which the same mutation type (numbers of CAG mutations in neurons) can cause symptoms over a 20 year range. Too bad that headlines are inherently short and sometimes misleading. Simple sells.
- pedalpete 2y agoThe problem with the amyloid hypothesis is most likely not that it is wrong, but that it is incomplete, and I would say that is the problem with this test as well. I work in neurotech/sleeptech, and AD researchers are using (or want to use) slow-wave enhancement to prevent and possibly manage AD. However, the test for AD is still a psychological tests along with neuroimaging to look for tau tangles and amyloid plaque build up. It has been discussed that we may be looking at multiple different diseases which have similar symptoms and without completely understanding the disease itself, we are categorizing them as AD, though they may have different pathways. Though we can't ignore the challenges to the amyloid hypothesis, we also shouldn't completely throw it out. Most of the experts I've spoken with still believe it is the best hypothesis we have, but that we also should not ignore other possibilities.
- everdrive 2y agoUntil we have a way to actually treat Alzheimer's, this seems like a mixed blessing at best. I suppose you could get your affairs in order, you but won't be enjoying much of those 10 years.
- RhysU 2y agoWhy does one need a looming Alzheimer's issue to get one's affairs in order? Wills, etc should be done decades before that stage of life. As soon as one has any spouse or dependents one should do all that jazz.
- codingdave 2y agoThere would be a different level of detail if you knew for a fact you were going that direction. Living wills and power of attorney are often fairly generic, as you don't know what situation will arise that will make them necessary. Well, now you would know a specific likely scenario, and you can get specific about each step of the expected progression. You may even change your financial plans - you would know that you need to get all the life you can out of the next 10 years, and you know you will have above average costs for medical care after those 10 years. I do not envy the work/life balance decisions to be made in such a scenario, but at least you get the opportunity/burden to make them.
- deleted 2y ago[deleted]
- pedalpete 2y agoThere are multiple pharmaceuticals which are used to slow the progression of the disease. We're in the neurotech/sleeptech space and have been developing slow-wave enhancement tech for the last few years, our technology is beginning to be used in clinical studies. These studies (using other less effective devices) have shown promise https://pmc.ncbi.nlm.nih.gov/articles/PMC10758173/ https://pmc.ncbi.nlm.nih.gov/articles/PMC10758173/ https://jcsm.aasm.org/doi/10.5664/jcsm.10778 https://jcsm.aasm.org/doi/10.5664/jcsm.10778
- yowayb 2y agoIt was always strange to me that scientists (people that are expected to be rigorous in their experimentation and analysis) would not include history in their analysis. However, the Latin root of the word "science" is about cutting or taking something apart and zooming in. Perhaps another word is needed to describe the process of putting whatever is scientifically discovered within a larger context to account for so many variables that are ignored during the scientific process. I personally suspect that all the biomarker stuff are really just the biochemical remnants of processes that begin at the sociocultural level.
- DiscourseFan 2y ago>I personally suspect that all the biomarker stuff are really just the biochemical remnants of processes that begin at the sociocultural level. That is a bit extreme. The sun is still set to die out in five billion years, regardless how much we talk about it. Its entirely possible that Alzheimer's has an origin which goes beyond any specific social circumstance, though I doubt it.
- gsf_emergency_2 2y ago"Math"? As argued in https://news.ycombinator.com/item?id=43053625 https://news.ycombinator.com/item?id=43053625 Etymology: "learning"
- kanavs 2y agoAt my company, we have been looking at understanding how the beta-amyloid interacts with toxic metals in the brain that lead to formation of plaques. We have been studying the use of quantum computers for such complex reactions. Most of us come from quantum computing and quantum chemistry background, so, relatively low experience with biological aspects. And as we dug deep into the reactions and made some good progress, a few established biologists got interested and asked questions around the beta-amyloid hypothesis itself. So, I dug a little deep into the whole field, most of my information comes from the following article: https://www.science.org/content/blog-post/faked-beta-amyloid-data-what-does-it-mean https://www.science.org/content/blog-post/faked-beta-amyloid... After doing some independent reading, following were my big take aways: - figuring out the truth in this area is incredibly hard. Science already suffers from social quirks like, scientists find it easy to say, 'hey, we replicated the decades-old established results and built something on top of it' rather than risk shaking the fundamentals of the field. All the big shots who did research on Alzheimer's got a lot of money from NIH for decades. Most of the projects were around beta-amyloid and these grants do not stop. So, if suddenly the field agrees that the hypothesis is incorrect, then a lot of people would lose jobs and livelihoods overnight. So, it is not just a scientific problem, the social-economic elements are quite powerful in this field. - Another fascinating thing I learned was that at this point Alzheimer's and beta-amyloid are quite intertwined. In fact, if a patient has Alzheimer's like symptoms but does not have a high concentration of beta-amyloid plaques then, the doctors may bucket such symptoms another form of dementia, with high probability. Coming from a Physics background, I found it incredibly fascinating that we depend on some loose markers and symptoms to define such complex diseases. And as you may have noticed from some of your personal experiences, symptoms sometimes can overlap in diseases and many times not everyone experiences the same symptoms and in fact a single human may experience different symptoms from getting the same disease. - So bottom line, not only we do not fully understand the pathophysiology of Alzheimer's, but there's a chance that we do not even understand what even is Alzheimer's.
- absolutelastone 2y agoThere's grants and studies going on for all kinds of treatments for Alzheimer's. Amyloid may be the biggest category, perhaps undeservedly, but it's still a minority of them. Also I think your article may be a bit out of date. Haven't there been more successful studies recently? I certainly agree about how weak the "ground truth" really is when it comes to these diseases. The theories are necessarily always going to be highly simplistic models that are ultimately wrong but sometimes useful. The only real causation they can show is from studies which show a drug works. And even then they usually don't really understand why (though it's human nature to think that if you can predict something successfully your theory is proved to be true).
- miika 2y agoThere was this super interesting new research.. https://www.sciencealert.com/alzheimers-may-not-actually-be-a-brain-disease-an-expert-reveals https://www.sciencealert.com/alzheimers-may-not-actually-be-... Alzheimer's may not be primarily a brain disease but rather an autoimmune disorder where the brain's immune system mistakenly attacks its own cells, with beta-amyloid playing a central role. There is a growing consensus that focusing solely on beta-amyloid has led to stagnation in treatment development, prompting researchers to explore alternative theories and treatment pathways. Also there is potential fabrication of data in a key 2006 study linking beta-amyloid to Alzheimer's and the FDA's approval of aducanumab, which has faced criticism for its incomplete data.
- buovjaga 2y agoThis is about a new cerebrospinal fluid assay. These days there are also blood tests, which are obviously way easier to take and much less unpleasant: https://www.nature.com/articles/s41591-024-02869-z https://www.nature.com/articles/s41591-024-02869-z https://www.fujirebio.com/en/products-solutions/lumipulse-g-ptau-217-plasma https://www.fujirebio.com/en/products-solutions/lumipulse-g-...