Mattsson N, Insel PS, Palmqvist S, Stomrud E, van Westen D, Minthon L, Zetterberg H, Blennow K, Hansson O. Increased amyloidogenic APP processing in APOE ɛ4-negative individuals with cerebral β-amyloidosis. Nat Commun. 2016 Mar 7;7:10918. PubMed.

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  1. Interestingly, last year, in Maia et al., we have shown that in three different APP transgenic mice, Aβ deposition seems to be ruled distinctively. In the initial stage of amyloid build-up, increased processing of APP seems more relevant, and in the second stage of amyloid progression sequestration outbalances production. This is true for both Aβ40 and 42.

    Our results are particularly curious since we were able to depict an increase in both CSF Aβ peptides, coincident with the start of Aβ deposition and before the massive amyloid deposition in all three mouse models studied. It would be interesting to assess if in this set of patients a similar biphasic profile occurs, as this would constitute a major finding with clinical implications: the earliest biomarker change in pre-clinical AD potentially impacting patient stratification and patient selection for clinical trials in pre-clinical AD. 

    References:

    Maia LF, Kaeser SA, Reichwald J, Lambert M, Obermüller U, Schelle J, Odenthal J, Martus P, Staufenbiel M, Jucker M. Increased CSF Aβ during the very early phase of cerebral Aβ deposition in mouse models. EMBO Mol Med. 2015 May 15;7(7):895-903. PubMed.

    View all comments by Mathias Jucker

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