Prana (PRAN) Reports Publication of Positive Data for PBT2 on Restoring Cognitive Function in Alzheimer's Patients
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Prana Biotechnology (Nasdaq: PRAN) reports The Journal Of Neurochemistry has published an update on the mechanism of action of PBT2 in the treatment of Alzheimer's Disease (AD). The study explains how PBT2 is able to restore cognition in AD sufferers through repair of affected Alzheimer's brains.
The findings further explain the rapid improvement in cognition previously reported in transgenic Alzheimer's mice and in patients in a Phase IIa clinical trial with PBT2.
The article published in the peer-reviewed Journal of Neurochemistry** is entitled "The Alzheimer's therapeutic PBT2 promotes amyloid-B degradation and GSK phosphorylation via a metal chaperone activity."
The study findings are particularly timely as Prana is about to start two clinical studies, one in AD and one in Huntington's Disease.
According to Prana's Head of Research, Associate Professor Robert Cherny, PBT2 provides a unique combination of detoxification and neuronal restoration to bring about the cognitive improvement observed in patients. It prevents Abeta oligomer formation, and delivers neurologically active metals (copper and zinc) into neurons damaged in AD.
This new data shows that delivery of these metals triggers intracellular molecular pathways which lead to improved cognition and increased expression of neuronal markers.
"Our findings indicate that PBT2 causes phosphorylation of the key cellular kinase, GSK3 by inhibiting the activity of the phosphatase, calcineurin, and refine our understanding of the mechanism of action of PBT2. Both GSK3 and calcineurin are viewed as important targets for AD therapies," Dr. Cherny stated.
Activation of this pathway also explains how PBT2 caused the large decrease in hyperphosphorylated tau, a brain protein associated with AD.
The findings further explain the rapid improvement in cognition previously reported in transgenic Alzheimer's mice and in patients in a Phase IIa clinical trial with PBT2.
The article published in the peer-reviewed Journal of Neurochemistry** is entitled "The Alzheimer's therapeutic PBT2 promotes amyloid-B degradation and GSK phosphorylation via a metal chaperone activity."
The study findings are particularly timely as Prana is about to start two clinical studies, one in AD and one in Huntington's Disease.
According to Prana's Head of Research, Associate Professor Robert Cherny, PBT2 provides a unique combination of detoxification and neuronal restoration to bring about the cognitive improvement observed in patients. It prevents Abeta oligomer formation, and delivers neurologically active metals (copper and zinc) into neurons damaged in AD.
This new data shows that delivery of these metals triggers intracellular molecular pathways which lead to improved cognition and increased expression of neuronal markers.
"Our findings indicate that PBT2 causes phosphorylation of the key cellular kinase, GSK3 by inhibiting the activity of the phosphatase, calcineurin, and refine our understanding of the mechanism of action of PBT2. Both GSK3 and calcineurin are viewed as important targets for AD therapies," Dr. Cherny stated.
Activation of this pathway also explains how PBT2 caused the large decrease in hyperphosphorylated tau, a brain protein associated with AD.
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