Santa-Maria I, Hernández F, Del Rio J, Moreno FJ, Avila J.
Tramiprosate, a drug of potential interest for the treatment of Alzheimer's disease, promotes an abnormal aggregation of tau.
Mol Neurodegener. 2007;2:17.
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Lest this become the "Jurgen Gotz solo" stage, I'd like to sound my three notes:
First, to thank Lon Schneider for his most enlightening dissection of the problems surrounding the Alzhemed trial. To be honest, while I had hoped for the best, I am not really surprised by the outcome of the Phase III because Alzhemed could not be labeled a "disease-modifying" compound—at the most pathology-modifying.
Second, to recommend the study by Santa-Maria and the group of Jesus Avila, for indicating another problem with the compound, totally overlooked—or rather invisible—in amyloid model mice! Actually, we do not understand tau dynamics well enough yet to predict if the tramiprosate effect on tau will be a problem or not, but it needs to be studied. The study stresses once again the importance of realizing that AD is invariably amyloid and tau pathology combined and the pre-clinical models must reflect that fact.
Third, to congratulate AlzForum for bringing this story and showing us all sides of it.
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