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01/16/2020

To give an example of how this works, the following are three articles published recently.

To give an example of how this works, the following are three articles published recently.
One of them, “The role of the immune system in the pathogenesis of Alzheimer’s disease” published in Nature Medicine, has been reported widely: in the news, on blogs, in the press, and the general media have described it in a lot of headlines. The following is a quote, from the abstract (boldface with my emphasis):
“A striking aspect of the current study is that the role of the immune system in the pathogenesis of Alzheimer’s disease has been completely overlooked. The discovery that increased Treg expression is required for amyloid plaques to form, and thus that Treg mediated anti-inflammatory mechanisms could be causally relevant in Alzheimer’s disease, could be the foundation for therapeutic intervention in this age-related disease. This is a major breakthrough that opens exciting new clinical horizons for Alzheimer’s disease.”
The second one is “Autism Spectrum Disorders and the Neuroinflammation Hypothesis” published in Neurobiology of Aging.
Although this article has been published since 2002, but the headlines of the recent articles (even as far as a couple of years down the line) are similar to the first one.
This one in particular is very popular in the press, because it is an updated version of “Pigments of the Immune System and Alzheimer’s Disease”…
It is in this context that we cannot be surprised to find that a few media outlets got this wrong. That was not the case before the publication of “The role of the immune system in the pathogenesis of Alzheimer’s disease”.
Another related article (1, 2) that was also reported in recent news outlets, was “Autism spectrum disorders and the neuroinflammation hypothesis.” The authors claimed that “neuroinflammation is a hallmark of Alzheimer’s disease” and that “pigments of the immune system” played an important role in this process.
These two articles got many other headlines, too, like “Autism and Alzheimer’s diseases shared similar triggers: studies”, “Neuroinflammation: the common denominator in autism and Alzheimer’s”, “Study links autism to inflammation”.
The only difference is, in the first article a correction was quickly published (3) (after 2 years of reports), stating that the authors were wrong: “Pigment of the immune system triggers brain inflammation” was not the case.
And I don’t agree with this correction. The authors did not “sting” any mice by injecting different colors of fluorescing protein, for instance. Or by forcing-feed them the “pigments of the immune system” (i.e. by injecting the antigenic protein). Instead, they simply induced the mice to develop an inflammatory state.
A mouse with Tg-Amyloidosis would be injected with a fluorescent protein from the culture which was colored blue, green, or red-orange. The injection of these fluorescent proteins will induce the mice to develop increased inflammation (the mice will develop red-fever, for instance), and when this increased inflammation reaches a certain point, the mouse will be labelled as “pigment of the immune system” – hence called blue Tg Amyloidosis.
And, as we have mentioned a few times before (e.g. “Autism spectrum disorders and