It's important to remember that there is growing doubt that amyloid plaques are that important to Alzheimer's disease, or at least that they are a direct cause.
Here is a Nature news story explaining some of the controversy:
In short, it seems Amyloid plaques can be found in the brains of many people who died of old age without developing any kind of dementia, and there are people with advanced Alzheimer's disease and almost no amyloid plaques at all; and there has been no success whatsoever in even slowing the disease with drugs that reduce the levels of amyloid plaques.
The debate seems to be pretty complex. From that article:
>Critics of the hypothesis note that the brains of many people who did not have Alzheimer’s disease have been shown to contain plaques on post-mortem. And they point to the failure of many clinical trials of treatments designed to dissolve amyloid plaques, none of which has slowed the disease. Researchers who support the amyloid theory counter that although the density of the plaques varies a lot between individuals, the density of tau tangles that they trigger correlates tightly with the severity of disease. And clinical trials probably failed, they say, because the treatments were given too late in the course of disease.
>They also have strong evidence on their side. There are certain rare and aggressive forms of Alzheimer’s disease that emerge early — between the ages of 30 and 60 — and run in families; these conditions are caused by mutations in genes that govern the amyloid-making process and inflammation in the brain. Scores of other genes have been associated with the risk of the more common late-onset form of the disease. Several code for proteins that comprise elements of the amyloid cascade, and some are involved in the innate immune system — a group of mechanisms that activate quickly to prevent the spread of pathogens in the body, and which drive inflammation.
Yeah, even with those limitations, it's still possible that the relationship between plaque buildup and Alzheimer could be similar to the one between smoking and lung cancer - you can get the latter without the former (randomly or triggered by other causes), you can have the former without getting the latter, but in most people, the former will massively increase the risk of getting the latter. Then again, the plaque could also be a co-symptom caused by some third factor. We'll see eventually
The debate is complex, but the amyloid plaque people have been steamrollering everybody else into submission--which is unfortunate as their hypothesis has failed every single time it has been put to the test.
However, Big Pharma is no longer backing amyloid plaque research because every single drug targeting them has failed for Alzheimer's.
At this point, it's very likely that amyloid isn't the problem. It's probably a response--and likely one that occurs long after the damage is done.
This is interesting because it’s another application of Cu64 for PET imaging as opposed to more widely available tracers such as F18 or Ga68. Cu64 has some advantages because it has a comparable positron energy to F18 which leads to good image resolution but a substantially longer half life at 12 hours, which makes logistics of dose delivery and radiopharmaceutical preparation much easier than the 110 minute half life of F18.
Cu64 has recently been approved as the radionuclide pair for neuroendocrine tumor imaging in Cu64-Dotatate so hopefully we see more agents coming online.
The isotope of copper known as CU64 is used for seeing what is happening inside the body. When CU64 decays back into normal copper, it emits a particle called a positron, which passes through the body and we can detect. By putting CU64 inside the body we can see things like internal organs where the copper accumulates. This is called positron emission tomography, or a PET scan.
CU64 is one of many isotopes you can use for this, and is nice because unlike other options it emits a good quantity of particles (resulting in good image quality) and lasts a long time (so we don’t have to worry about it getting to where it needs to be - in the world and in the body - before it decays).
The picture of the main author should appear first, his picture should be larger, and this should read "Research scientist Hong-Jun Cho and his colleages". Same as the paper.
If he's the first author, he's probably not the lab PI, and the PI usually gets the public credit, not the first author. Lab politics. Thats a complication with the research system as a whole, not with this particular news piece
"The way this is reported truly sucks. The picture of the main author should appear first, in my opinion. And this should read "Research scientist Hong-Jun Cho and his colleages""
Except in science the last author of the paper is the most significant one. So the way this article is written is just right.
It depends on the field (and journal, author preferences, and a bunch of other things...), but the main author is generally the person who did the bulk of the research and the last author is the usually the principle investigator, group lead, or gatekeeper (i.e., the person who frames the paper for a particular journal(s) to maximize publication success).
As far as how all of this played out in this case, who knows, but I don't see anything particularly wrong with having either the first author or group lead as the main focus of the article, as long as both of them (and the other contributors) are openly acknowledged, which appears to have happened.
This one is interesting, cause it really depends who you mean by "significant" The first author is generally the primary researcher. The last author is generally the PI of the entire lab, and the person of highest status in the lab.
Use $15 worth of hireable Photoshop to create a decent looking image with all of them? Even just squares of profile photos put together, but I almost guarantee a better job could be easily done.
There are four authors in that paper. Just because there are papers that contain 100s of authors should not influence this specific case of a four author paper.
Here is a Nature news story explaining some of the controversy:
https://www.nature.com/articles/d41586-020-03084-9
In short, it seems Amyloid plaques can be found in the brains of many people who died of old age without developing any kind of dementia, and there are people with advanced Alzheimer's disease and almost no amyloid plaques at all; and there has been no success whatsoever in even slowing the disease with drugs that reduce the levels of amyloid plaques.