From Pitor on the Yahoo MB "
Piotr
42 minutes ago
It seems that A2-73 beats the crap from anything in Ad field but the data for both A2-73 Alone and A2-73 with DPZ up to 31 weeks does not support that. Well, may be with the exception of sudden gain in MMSE scores for A2-73 Alone patients where after 18 weeks there was a harbinger of things to come at 57 weeks for all patients, that is the current PR end results. Yet, they without the the understanding how the data differ for the two groups of patients and their plot versus time is not giving indications of the AVXL's achievment.
All patient data up to 31 weeks for the functional measures is declining with the disease free progression or even worse. The plot can be obtained from measuring the positions of data points on the poster of 31 week data and doing some weighted additions and divisions to get a mean. No wonder, that AVXL divided the data into groups and that presented it without reference to AD free progression. The only glimps of a light at the end of the tunnel was the jump in MMSE (cognitive) score at 31 weeks for A2-73 Alone patients. The functional scores, ADCS-ADL, for A2-73 alone patients rose in first 5 weeks and then declined witht the rate of the disease, that data is available only till 31 weeks. Since at 31 weks the cognitive score soared I expect the functinal A2-73 Alone scores to follow suit at 57 weeks. After 31 weeks functional scores for all patients went up to difference of 4 points over free progression, making sudden revearsal of the trend down, because there was a preceeding cognitive scores moonshot this should be genuine. The same has happened to 57 weeks cognitive scores for all patients, that is reversal of a trend down into scores improving greatly over DPZ and disease. From the pure stand of arithmetics the improvements must happen in both groups of the patients with the A2-73+DPZ lagging A2-73 Alone and conginitive leading the functional. It is obvious by now that the change in language by AVXL to inclusion of the word homeostasis in light of the forced solution of MOA of DPZ that is "This results in an increased acetylcholine concentrations at cholinergic synapses." as we can read in Wikipedia. This might be just throwing a monkey wrench into fragile homeostasis in AD. It seem to papper over the underlying cause of the disease.
If the trend reversal is permanent then it might be indeed the cure but farther data might or not corroborate the staying power of that new trend.
see tweets for illustrations.
Comments??? Rebuttal ????
