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Thursday, February 09, 2017 7:44:32 AM
Patient was subjectively judged by others to have experienced limited improvement of symptoms that persisted for 8 weeks. I'm assuming that 8 weeks was for the first couple of months of treatment. Not sure if he was on other Alzheimers drugs at the time. No mention of side effects. No hard data given. Patient's symptoms were so far advanced that I doubt he was capable of participating in typical cognitive assessment tests. No mention of brain scans, P300, erp's, or any testing whatsoever.
The 8 weeks of improvement, was that during treatment, or was that improvement that persisted for 8 weeks after treatment had ended? Did all 3 compassionate use patients have early onset Alzheimers caused by rare expression of the same gene? If so, is the mechanism that caused their atypical expression of Alzheimers related to the cause of Alzheimers in most patients? For instance, does the rare expression of that gene in that family perhaps cause an enzyme (for example, PKC) not to function properly, resulting in this rare, very early onset, expression of severe Alzheimers? Is it unlikely that this is the same mechanism that causes Alzheimers in most patients? If bryostatin targets that mechanism, would it also be expected to work in patients that develop Alzheimers due to a different mechanism?
http://www.j-alz.com/content/severe-alzheimers-patient-responds-bryostatin-treatment
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