Alzheimer’s treatment appears to alleviate memory loss in small trial
nature.com
nature.com
It seems like these types of drugs are best used for prevention rather than a cure, so I've been taking it for a year or so now even though I'm not even 30, and plan to continue for the rest of my life. I've lost quite a few relatives to Alzheimer's/dementia, so it is pretty cheap "insurance" to me, even if it turns out it just makes expensive pee.
If the long-term protective benefit of the otc drug specifically as it relates to AD has not been studied, don't start taking it under 30.
What has been studied are the links between your lifestyle and both protection from disease onset, and maintenance of cognitive function at the highest possible level throughout the early stages of disease. Stay smart. Always learn. Be physically active. Challenge yourself.
Also, as treatments emerge over the next 30 years, the barrier to adoption will be the social stigma and an education problem. People don't want to get diagnosed for Alzheimer's Disease. Geriatric Psychs lament that family members are bringing in their loved ones nearly 100% of the time. Preventative drugs, as they become available, need to be taken early, yet, the earliest phases of the disease are difficult to disambiguate from normal cognitive decline that occurs with aging. Add in the fear - you just don't want to know - and you get most patients arriving to diagnosis too late. You're already on the right track by being confident, proactive, and taking responsibility to do what you can to remain as healthy as possible throughout your life. Don't stop.
https://www.statnews.com/2016/04/12/alzheimers-disease-colom...
Perhaps you should participate in a study, if possible? There's an interesting documentary on HBO:
http://www.hbo.com/alzheimers/about-the-project.html
I believe BioGen's drug is discussed in the movie.
Another very important preventative (and even sometimes disease-reversing) measure for Alzheimers is teaching your body ketosis by consuming little to no carbs, eating more good natural fat and never ever touching processed ("low-fat") foods. It is believed that Alz. is inability of brain cells to metabolize glucose, but with ketosis they can power themselves with ketone bodies just as well.
An obligatory reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/
Curiously, humans may be the only (or one of very few) species capable of ketosis: http://caloriesproper.com/ketosis-in-an-evolutionary-context...
"We conclude that the term "type 3 diabetes" accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM."
If that's correct, it's also a demonstration that removing the plaques doesn't remove the cognitive impairment.
I didn't know this was possible. Is it ?
If they are a symptom then that explains why removing them doesn't change anything.
There is a large phase 3 trial going on now https://www.clinicaltrials.gov/ct2/show/NCT02477800 but we won't know the results for several years. They are still recruiting patients, so if you or someone you know has early stage Alzheimer's, it's worth considering.
But if you dive deeper you realize that they have not demonstrated cognitive benefits. In other words, it might not do anything. So what, you say, I still want to try it.
Then you look and you see that 40 people (roughly a quarter) had to leave the trial because of fluid build up in their brains, that could cause brain bleeds.
No cognitive benefits and brain bleeds would be a sad outcome.
http://www.nature.com/nature/journal/v537/n7618/full/nature1...
Maybe there's free news coverage somewhere on Nature.com
Article/Study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221920/
Interventions: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221920/table/T1...
Presentation by the doctor: https://www.youtube.com/watch?v=QqQ_X3mD16U
For some context, I read in the book "Peak" by Anders Ericsson (who is credited with the 10000 hour rule) [1] that cab drivers in London who passed the cab exam literally rewired their brains during the process of studying and it could be observed in the brain scans. (But also notes that they unfortunately lost some spatial awareness ability which the average person had)
[1] https://www.amazon.com/Peak-Secrets-New-Science-Expertise/dp...
http://www.nature.com/news/alzheimer-s-treatment-appears-to-...
Other references:
Publicity materials: http://www.eurekalert.org/pub_releases/2016-08/uoz-arh083016...
Paper (not open access): http://dx.doi.org/10.1038/nature19323
Alzheimer's disease research is perhaps the largest single theme in the aging research community, with the majority of National Institute on Aging funding going towards Alzheimer's programs. The most advanced of efforts in Alzheimer's research are those that seek to clear the accumulation of amyloid-β in the brain through the use of immunotherapies, enlisting the immune system to break down and remove the unwanted amyloid. To date, however, this has proven to be a road of great expense characterized by disappointment and slow progress, to the point at which it was possible to question whether amyloid was the right target. Other theories and lines of research have begun to prosper due to the lack of tangible human results for anti-amyloid immunotherapies, in particular that neurofibrillary tangles of misfolded tau protein are just as much a target for clearance as is amyloid-β, and that perhaps it is time to focus on the decline of known clearance mechanisms rather than the amyloid itself.
Still, over the past couple of years, one of the latest entries to the class of anti-amyloid immunotherapies has lived up to some of the promise first seen in animal studies of amyloid clearance. It may well be that the light at the end of the tunnel is in sight. In a human trial that has now lasted a year, this new immunotherapy cleared near all detectable amyloid-β from patients, and the patients showed improvement in the sense that their decline appeared to slow significantly. The caveat here is that a year is not long enough to declare a slowing of the condition in certainty given the number of people treated in the trial, 165 individuals. Certainty will arrive given time and more patients. Regardless, simply through the demonstrated clearance of amyloid in human patients this is a big step forward for the field. If this holds up over the next few years of larger trials it should become very clear as to the degree to which amyloid-β is or is not in fact the primary cause of pathology in Alzheimer's disease.
I have long said that the best way to answer these questions of cause and contribution is to remove the mechanism in question and see what happens. As an approach that is much, much faster - and thus more cost-effective - than trying to infer the answer by analyzing the enormously complex workings of cellular biochemistry. This principle is well demonstrated here in the matter of amyloid, I think, given the past decade of theorizing on the degree to which the harm of Alzheimer's is due to amyloid, tau, or other causes, and the lack of progress on that front from theorizing alone. As soon as a treatment can reliably and safely remove the amyloid from a sizable number of Alzheimer's patients, we will have the answer.