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Wednesday, July 17, 2019 1:45:49 PM
A few thoughts on what was presented:
1) "ANAVEX®2-73-Treated Patients have higher Abundance of Bacteroidetes and Firmicutes Phyla in Gut Microbiota"
Good - Additional biomarker confirmation that the A2-73 treated patients do have AD and thus further helps to eliminate misdiagnosis.
2) "KEM® Identifies Changes in two Gut Microbiome Families - Ruminococcaceae and Porphyromonadaceae - Associated with Response to ANAVEX®2-73"
On the face of it seems meaningful delta ADCS-ADL increase in the High concentration patients with a relative abundance of the two KEM covariant bacteria families identified, but as usual it leaves some unanswered questions, at least in my mind:
- There is an enormous spread in response among the 14 patients (of 16 providing stool samples) especially among the High concentration Delta ADCS-ADL scores. Why - and how does this correlate with the spread in response in the high concentration group excluding the Gut analysis?
- Not sure I understand from this representation the relative importance to response of the two bacteria types?
- Does it mean just as little in terms of meaningful clinical benefit as the SIMGMAR1 and COMT1 variant genes?
- At least for the gene variants we got charts showing that although highly stat sig the outcome difference was minute.
- Why not similar charts for this analysis?
This PM stuff to me seems a bit like fashionable dressing cloaked in a lot of words.
1) "ANAVEX®2-73-Treated Patients have higher Abundance of Bacteroidetes and Firmicutes Phyla in Gut Microbiota"
Good - Additional biomarker confirmation that the A2-73 treated patients do have AD and thus further helps to eliminate misdiagnosis.
2) "KEM® Identifies Changes in two Gut Microbiome Families - Ruminococcaceae and Porphyromonadaceae - Associated with Response to ANAVEX®2-73"
On the face of it seems meaningful delta ADCS-ADL increase in the High concentration patients with a relative abundance of the two KEM covariant bacteria families identified, but as usual it leaves some unanswered questions, at least in my mind:
- There is an enormous spread in response among the 14 patients (of 16 providing stool samples) especially among the High concentration Delta ADCS-ADL scores. Why - and how does this correlate with the spread in response in the high concentration group excluding the Gut analysis?
- Not sure I understand from this representation the relative importance to response of the two bacteria types?
- Does it mean just as little in terms of meaningful clinical benefit as the SIMGMAR1 and COMT1 variant genes?
- At least for the gene variants we got charts showing that although highly stat sig the outcome difference was minute.
- Why not similar charts for this analysis?
This PM stuff to me seems a bit like fashionable dressing cloaked in a lot of words.
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