Best AD yet this year http://finance.yahoo.com/q?s=PRAN If our executive management was smart, they would plunk down $200 M on this... we'll see if Pfizer gets there first.
Great Alzheimer's news
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Prana's PBT2 -- Directly Restores Neurons Critical to Cognition
PLoS ONE Publication on PBT2 Consolidates the Underlying Mechanisms for the Preclinical and Clinical Benefits of PBT2 in Alzheimer's Disease
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Press Release Source: Prana Biotechnology On Monday March 21, 2011, 11:30 am EDT
MELBOURNE, AUSTRALIA--(Marketwire - 03/21/11) - Prana Biotechnology (NASDAQ
RAN - News) (ASXBT - News) today announced the publication of new data on the ability of PBT2 to repair the damage in an Alzheimer's affected brain thereby facilitating the restoration of cognition in Alzheimer's Disease (AD). The findings help to 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 science journal PLoS ONE is entitled "Metal Ionophore Treatment Restores Dendritic Spine Density and Synaptic Protein Levels in a Mouse Model of Alzheimer's Disease."
The authors led by Dr Paul Adlard, Head of The Synaptic Neurobiology Laboratory at The Mental Health Research Institute, describe the biochemical and anatomical changes occurring in the brains of transgenic*** Alzheimer's mice treated with PBT2.
After 11 days of treatment, the brains of the Alzheimer's mice showed a statistically significant increase in the numbers of spines on the branches (or dendrites) of neurons in the hippocampus, a memory centre specifically affected in AD. Increasing the number of spines is important as this permits many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions.
Importantly, these anatomical changes to the hippocampus were also accompanied by increased levels in key proteins**** involved in learning, memory and neuronal growth. The levels of many of these proteins were restored to the levels seen in healthy, cognitively normal animals.
"The ability of PBT2 to promote the forming and reforming of connections between neurons is fundamental to the repair of brain tissue damaged by AD, and the expression of key neuronal receptors and signaling proteins indicates that the repaired tissue is functional," noted Prana's Head of Research, Associate Professor Robert Cherny.
In a series of parallel experiments, the authors also administered PBT2 to cultured neurons. In these in vitro experiments, PBT2 was able to elicit elongation of 'arm like' projections from the immature developing neurons called neurites. These projections can ultimately mature into either axons or dendrites of an adult neuron. Significantly, the changes observed in the in vitro experiments were strictly dependent on the presence of copper or zinc in the growth medium, confirming that the restorative effect of PBT2 is due to its ability to deliver these metals to deficient neurons.
It has previously been shown that PBT2 neutralises the toxicity of the Alzheimer's Abeta protein by preventing the formation of toxic aggregates or oligomers*. These new results further explain how PBT2 can achieve such rapid improvements in cognition: by liberating copper and zinc trapped in amyloid deposits and returning those essential metals to neurons, where they are needed for normal function.
"These findings further demonstrate the unique combination of detoxification and neuronal restoration provided by PBT2 that underlie cognitive improvement in the clinic," concluded Dr Cherny.
PLoS ONE Publication on PBT2 Consolidates the Underlying Mechanisms for the Preclinical and Clinical Benefits of PBT2 in Alzheimer's Disease
marketwire
Companies:
Prana Biotechnology Limited
Prana Biotechnology Ltd
Related Quotes
Symbol Price Change
PBT.AX 0.1650 +0.0250
Chart for PRANA FPO
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Press Release Source: Prana Biotechnology On Monday March 21, 2011, 11:30 am EDT
MELBOURNE, AUSTRALIA--(Marketwire - 03/21/11) - Prana Biotechnology (NASDAQ
RAN - News) (ASXBT - News) today announced the publication of new data on the ability of PBT2 to repair the damage in an Alzheimer's affected brain thereby facilitating the restoration of cognition in Alzheimer's Disease (AD). The findings help to 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 science journal PLoS ONE is entitled "Metal Ionophore Treatment Restores Dendritic Spine Density and Synaptic Protein Levels in a Mouse Model of Alzheimer's Disease."The authors led by Dr Paul Adlard, Head of The Synaptic Neurobiology Laboratory at The Mental Health Research Institute, describe the biochemical and anatomical changes occurring in the brains of transgenic*** Alzheimer's mice treated with PBT2.
After 11 days of treatment, the brains of the Alzheimer's mice showed a statistically significant increase in the numbers of spines on the branches (or dendrites) of neurons in the hippocampus, a memory centre specifically affected in AD. Increasing the number of spines is important as this permits many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions.
Importantly, these anatomical changes to the hippocampus were also accompanied by increased levels in key proteins**** involved in learning, memory and neuronal growth. The levels of many of these proteins were restored to the levels seen in healthy, cognitively normal animals.
"The ability of PBT2 to promote the forming and reforming of connections between neurons is fundamental to the repair of brain tissue damaged by AD, and the expression of key neuronal receptors and signaling proteins indicates that the repaired tissue is functional," noted Prana's Head of Research, Associate Professor Robert Cherny.
In a series of parallel experiments, the authors also administered PBT2 to cultured neurons. In these in vitro experiments, PBT2 was able to elicit elongation of 'arm like' projections from the immature developing neurons called neurites. These projections can ultimately mature into either axons or dendrites of an adult neuron. Significantly, the changes observed in the in vitro experiments were strictly dependent on the presence of copper or zinc in the growth medium, confirming that the restorative effect of PBT2 is due to its ability to deliver these metals to deficient neurons.
It has previously been shown that PBT2 neutralises the toxicity of the Alzheimer's Abeta protein by preventing the formation of toxic aggregates or oligomers*. These new results further explain how PBT2 can achieve such rapid improvements in cognition: by liberating copper and zinc trapped in amyloid deposits and returning those essential metals to neurons, where they are needed for normal function.
"These findings further demonstrate the unique combination of detoxification and neuronal restoration provided by PBT2 that underlie cognitive improvement in the clinic," concluded Dr Cherny.
Thank you for that news.
Either this is a red herring, or it's a multibillion/year drug. PBT2. I wonder if we at Lilly have done any work on this ...
Either this is a red herring, or it's a multibillion/year drug. PBT2. I wonder if we at Lilly have done any work on this ...
Well with this kind of news, some of us may just end up with early retirement (our choice)
The common stock is only worth about 50 million. Seems like a "no-brainer" to me.
Hey small molecules have had a fabulous history in the prevention and treatment of human disease - here is one that seems effective in AD. If not outright purchase of the company, at least borrowing their ideas would be prudent.
Hey small molecules have had a fabulous history in the prevention and treatment of human disease - here is one that seems effective in AD. If not outright purchase of the company, at least borrowing their ideas would be prudent.
small biotechs survive on rumors -- not on science.
Now, if FDA were to approve drugs for mice, nearly 45% of all compounds in US pharmacopoieae would work exactly as observed. Problem is that mice to rat to dog/cat to chimp/rhesus > human Ph1 is 97% loss of the compounds due to toxicity/metabolism issues.
Mice (nude and other congenics) are so by design to see observed effect.
Human population is so varied (epigenomically) that some drug acting at age 56 may not work at 66 or may work 200% more.
It is one thing to show effects in mice and in Phase 3 clinical trials, to have drug work for more than three months without side effects is nearly impossible, unless epigenomic modifications are controlled, in which can we can control aging and ensuing illnesses.
"Drug candidates clioquinol (CQ) and PBT2 (Prana Biotechnology Ltd) have a moderate affinity for metal ions, and rather than deplete biological metals in cell culture, promote the uptake of Cu and Zn "
Now, if FDA were to approve drugs for mice, nearly 45% of all compounds in US pharmacopoieae would work exactly as observed. Problem is that mice to rat to dog/cat to chimp/rhesus > human Ph1 is 97% loss of the compounds due to toxicity/metabolism issues.
Mice (nude and other congenics) are so by design to see observed effect.
Human population is so varied (epigenomically) that some drug acting at age 56 may not work at 66 or may work 200% more.
It is one thing to show effects in mice and in Phase 3 clinical trials, to have drug work for more than three months without side effects is nearly impossible, unless epigenomic modifications are controlled, in which can we can control aging and ensuing illnesses.
"Drug candidates clioquinol (CQ) and PBT2 (Prana Biotechnology Ltd) have a moderate affinity for metal ions, and rather than deplete biological metals in cell culture, promote the uptake of Cu and Zn "
It's the proof of concept that is of value here. The previous approaches, taken by Lilly and Pfizer, were doomed to failure, and even then billions of dollars were spent. Here you have a much lower-risk study in terms of cost.
Human trials ARE underway.
Human trials ARE underway.
For the doubting thomas (who in complete idiopathic Lilly form, strikes down a good idea because it wasn't his) http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017669