The news item by Charles Piller just published in Science BLOTS ON A FIELD? A neuroscience image sleuth finds signs of fabrication in scores of Alzheimer’s articles, threatening a reigning theory of the disease highlights the recent news and activity around a series of papers discussion Aβ*56, a specific, proposed type of toxic oligomer of amyloid beta or Aβ.

There are questions of image altering and of the veracity of Aβ*56 isolation and measurements, and expressions of concern have been recently added to online versions of a numnber of papers referring to it going back to the 2006 Nature paper A specific amyloid-β protein assembly in the brain impairs memory.

Several drugs developed for treatment of Alzheimers Disease have targeted Aβ.

I'm having difficulty understanding how far the implications of the recent concern reaches. Is it simply the correlation with the particular form Aβ*56 associating with Alzheimers, or is it the connection between any oligomer of Aβ? Does the recent concern over several papers about it call into question the association of Alzheimers Disease with any Amyloyd beta oligomer forms?


1 Answer 1


Does the recent concern over several papers about Aβ*56 call into question the association of Alzheimers Disease with any amyloyd beta oligomer forms?

From my understanding, no. alzforum.org has many great comments on it, e.g. from David Brody:

In my own group, we tried replicating the Aβ *56 western blots for about a year, without success. We then moved on to other things.

Our later work on soluble Aβ aggregates/oligomers from human brain tissue indicated that they are considerably larger than Aβ *56 (Esparza et al., 2013; Esparza et al., 2016).

I think these larger soluble Aβ aggregates/oligomers may still be important potential therapeutic targets, but not Aβ *56.

The strongest evidence comes from the labs of Dennis Selkoe and Dominic Walsh.


or from Thomas Bayer:

In my view, Aβ-amyloid oligomers are valuable and realistic drug targets. However, not all Aβ oligomers described in in vivo or in vitro model systems do exist in human brain. Besides full-length Aβ, N-truncated Aβ peptides, pyroglutamate Aβ 3-42 and Aβ 4-42 represent a dominant fraction in the brains of patients with Alzheimer’s disease. Both N-truncated peptides show a high aggregation propensity to form stable aggregates as observed by NMR spectroscopy, for example (Bouter et al., 2013).


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    $\begingroup$ Thanks for the link - some very interesting comments on the blog post. One takeaway message from some of the comments is that the Science article contains some misguided views, so they are definitely worth reading to get a more well rounded picture of what happened; $\endgroup$
    – user438383
    Jul 25, 2022 at 21:09

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