Exact(1)
However, an Alzheimer sample (AD5) grouped with the PSP group (see Figure 1A).
Similar(59)
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.
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.
Using 83 of the samples, they measured the abundance of 120 proteins involved in cell signaling and found they could distinguish the Alzheimer's samples from the controls using 18 of the proteins.
The set GSE26927 included 11 samples with Alzheimer's disease, 10 samples with amyotrophic lateral sclerosis, 10 samples with Huntington's disease, 10 samples multiple sclerosis, 12 samples with Parkinson's disease, 10 samples with schizophrenia, and 55 control samples extracted from the entorhinal cortex; this dataset is based on the Illumina humanRef-8 v2.0 expression beadchip.
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.
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.
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