Change this to the nature article, it is much better. http://www.nature.com/news/alzheimer-s-treatment-appears-to-alleviate-memory-loss-in-small-trial-1.20509

Change this to the nature article, it is much better. http://www.nature.com/news/alzheimer-s-treatment-appears-to-alleviate-memory-loss-in-small-trial-1.20509 http://www.nature.com/news/alzheimer-s-treatment-appears-to-... Other references: Publicity materials: http://www.eurekalert.org/pub_releases/2016-08/uoz-arh083016.php http://www.eurekalert.org/pub_releases/2016-08/uoz-arh083016... Paper (not open access): http://dx.doi.org/10.1038/nature19323 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.