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In addition, methylation of another locus (SORBS3) was higher in the Alzheimer samples than in controls.
The FTD and PiD disease samples clustered as a single large group and four of five Alzheimer samples also clustered together.
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However, an Alzheimer sample (AD5) grouped with the PSP group (see Figure 1A).
On two separate test sets of 92 ("AD" Alzheimer's samples against control) and 47 ("MCI" mild cognitive impairment samples) the signature was able to show an overall effectiveness of 81% and 91% for AD predictability.
For example, we tagged Alzheimer's disease samples to AD1 whereas multiple sclerosis samples to MS1.
However when new Alzheimer's disease samples were also included, they did not cluster together with matching samples from the previous experiment, see Figure 2C.
In Alzheimer's disease samples no FOXO factor upregulation was observed, however as mentioned the AD samples and controls vary only on 11 genes, and the power to detect biologically relevant changes might be limited.
The age at death and post-mortem delay was not significantly different between the control and Alzheimer's disease samples.
The dataset GSE5281 comprises several distinct tissue subsets: EC - entorhinal cortex; HIP - hippocampus; MTG - Medial Temporal Gyrus; PC - Posterior Singulate; SFG - Superior Frontal Gyrus; VCX - Primary Visual Cortex, each being comprised of control and Alzheimer's disease samples.
Dephosphorylation of the sarkosyl-insoluble tau with lambda-phosphatase, followed by western blot analysis with a total tau antibody against all the isoforms, revealed the underlying isoform composition of the insoluble tau with a pattern similar to Alzheimer's disease samples (Fig. 2A).
Two of the studies in this review used a diagnosis-related sample (Alzheimer's disease), while the other two studies included participants with cognitive impairment of any type.
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CEO of Professional Science Editing for Scientists @ prosciediting.com