No Shit! The NY Times Almost Got it Right!


I work in an institute that specializes in neurodegenerative diseases. My mother knows this, and is fully scientifically illiterate, but will still send me the odd article which states “fascinating” and “provocative” findings, only to find that they either completely butchered the study, or were not even referring to a real scientific study at all. So, when she sent me a New York Times article entitled “Could Alzheimer’s Stem From Infections? It Makes Sense, Experts Say” I groaned, rolled my eyes and read on.

Score one for the NY Times, they actually linked the article! It usually takes me hours to find the original publication that everyone is referring to in the news. And, it’s published in Science. OK, I’m listening now. What does the article actually find?

A little background: Alzheimer’s Disease (AD) is a neurodegenerative disease which is precipitated by the formation of amyloid-beta plaques in the brain. These plaques are protein aggregates which pepper the brain tissue of the affected person. The problem is, once someone shows symptoms of AD, the plaques have already started forming and it is too late to do anything about it, therefore a lot of research into AD is dedicated to finding either (A) early warning signs, or (B) why the brain starts forming these plaques, in order to prevent them from even starting in the first place.

The question was, why do we even have amyloid-beta? It is a protein found in many animal species, indicating that it was highly conserved throughout evolution, but on the other hand it doesn’t seem to do anything other than cause trouble. Proteins don’t usually survive for hundreds of millions of years just to one day pop up to make sure our grandfather doesn’t recognize us when we come to visit. Do we even need amyloid-beta?

In this paper, they found a reason for the amyloid-beta to exist. It seems as though this protein is capable of protecting the brain from infections. When mice, worms and cells were exposed to certain infections, they secreted amyloid-beta, which engulfed the offending pathogen. Furthermore, mice which do not produce amyloid-beta were more likely to die of these infections than mice which did.

That’s super cool! There is a reason for amyloid-beta! Now, we need to see what molecular cues trigger the secretion, if they are the same molecular cues that trigger its secretion in patients with AD, and if we can somehow block those cues to prevent AD.

So, in conclusion, the NY Times kind of exaggerated a hypothesis that was presented in the discussion, and reworked the story to make it seem as though they found direct evidence that AD is caused by infection. In reality, it could be caused by the body “thinking” that it is infected when it’s not, it could be caused by a very mild infection that has yet gone unnoticed in studies of AD (though I doubt it) or it could be triggered by a completely different mechanism altogether. But, the link between AD and infections is there in the paper, although it is more indirect than the NY Times will lead you to believe.

Still, they did a hell of a lot better than newspapers usually do with science! I’ll give them a 7/10 on this one. Once in a while, my mother actually stumbles on a good story!

Comments

  1. dianne says

    This makes me wonder what would happen if you exposed these mice to PD-1 or PD-L1 inhibitors. Or ipi, for that matter. Could make the situation worse by increasing the inflammation or it could improve the situation by resolving the low level infection and allowing down regulation of the beta-amyloid protein.

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