. Apolipoprotein E, Neurodegeneration, and Alzheimer Disease. Arch Neurol. 2012 Dec 3;:1-2. PubMed.

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  1. This paper is very interesting. Longitudinal data will be the key to proving an anatomic pattern of progression, and the data here suggest a leading candidate hypothesis. These results are consistent with some findings we reported last year (Becker et al., 2011) relating amyloid more strongly to posterior cingulate/precuneus thinning of cortex than to hippocampal volume loss. The confound that many (including myself) are hoping to probe for this issue is the contribution of tau deposition in the medial temporal lobe versus other cortices. Ligands for that are coming.

    References:

    . FDG metabolism, amyloid deposition and APOE status in cognitively normal elderly subjects. Human Amyloid Imaging 2011 Meeting Abstracts. 2011 Jan 15;

    View all comments by Keith Johnson

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