Parkinson's Disease Tulip


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Old 05-11-2012, 07:48 AM #1
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Default Novel Alzheimer's drug that improved cognition in 12 week trial

PBT2 works on three metals in the brain:

Zinc
Copper
Iron
Copper & Zinc: In a recent presentation at ICAD, Prana's Head of Research, Associate Professor Robert Cherny, showed that the effectiveness of PBT2 lies in a unique combination of complementary activities. PBT2 acts to detoxify A-beta by disarming it of copper and zinc and returns these crucial metals to neurons. Dr. Cherny showed that by returning these metals to neurons, important cell signaling pathways are activated that prevent neuronal death and promote neuronal function. In addition, data was also presented linking the neuroprotective qualities of PBT2 with beneficial effects evident in an animal model of Huntington’s Disease.

Iron Overload: In additional research, evidence published in Cell shows that the source of beta-amyloid, the beta- amyloid precursor protein (APP), plays a hitherto unknown critical role in exporting iron out of neurons. If APP fails to carry out this role, iron builds up in the neurons contributing to oxidative stress, neurofibrillary tangle formation and ultimately neuronal cell death. Importantly, Prana scientists demonstrated that synaptic zinc can prevent APP from performing its normal iron transporting role. Synaptic zinc levels and distribution changes in the Alzheimer’s brain, because zinc released into the synaptic space is drawn into the beta-amyloid that forms plaques in the synapse. This is problematic for the brain because neurons are deprived of the zinc required for neurotransmission and the zinc induces toxic beta-amyloid oligomer formation. Moreover, as now indicated by the research in the journal, Cell, the zinc caught up in the beta-amyloid can be transported or exchanged to the APP, impeding its ability to prevent iron buildup in neurons.

Accordingly, the maintenance of correct zinc levels in the brain is vital for neuronal function and ultimately cognition.

Prana’s PBT2 acts as a zinc chaperone that transports zinc from the brain beta-amyloid deposits and returns it to neurons to facilitate normal neurotransmission. PBT2 has also demonstrated important neuroprotective and neurotrophic properties, consistent with its ability to prevent zinc from impairing the ability of APP to prevent iron overload.

http://alzheimersweekly.com/content/...-12-week-trial
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Old 05-11-2012, 08:10 AM #2
lurkingforacure lurkingforacure is offline
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Quote:
Originally Posted by olsen View Post
PBT2 works on three metals in the brain:

Zinc
Copper
Iron
Copper & Zinc: In a recent presentation at ICAD, Prana's Head of Research, Associate Professor Robert Cherny, showed that the effectiveness of PBT2 lies in a unique combination of complementary activities. PBT2 acts to detoxify A-beta by disarming it of copper and zinc and returns these crucial metals to neurons. Dr. Cherny showed that by returning these metals to neurons, important cell signaling pathways are activated that prevent neuronal death and promote neuronal function. In addition, data was also presented linking the neuroprotective qualities of PBT2 with beneficial effects evident in an animal model of Huntington’s Disease.

Iron Overload: In additional research, evidence published in Cell shows that the source of beta-amyloid, the beta- amyloid precursor protein (APP), plays a hitherto unknown critical role in exporting iron out of neurons. If APP fails to carry out this role, iron builds up in the neurons contributing to oxidative stress, neurofibrillary tangle formation and ultimately neuronal cell death. Importantly, Prana scientists demonstrated that synaptic zinc can prevent APP from performing its normal iron transporting role. Synaptic zinc levels and distribution changes in the Alzheimer’s brain, because zinc released into the synaptic space is drawn into the beta-amyloid that forms plaques in the synapse. This is problematic for the brain because neurons are deprived of the zinc required for neurotransmission and the zinc induces toxic beta-amyloid oligomer formation. Moreover, as now indicated by the research in the journal, Cell, the zinc caught up in the beta-amyloid can be transported or exchanged to the APP, impeding its ability to prevent iron buildup in neurons.

Accordingly, the maintenance of correct zinc levels in the brain is vital for neuronal function and ultimately cognition.

Prana’s PBT2 acts as a zinc chaperone that transports zinc from the brain beta-amyloid deposits and returns it to neurons to facilitate normal neurotransmission. PBT2 has also demonstrated important neuroprotective and neurotrophic properties, consistent with its ability to prevent zinc from impairing the ability of APP to prevent iron overload.

http://alzheimersweekly.com/content/...-12-week-trial
Thanks for posting this! I was feeling rather blue this week about the state of research and this has really helped lift my mood. I know they don't mention PD but given that a symptom of insufficient zinc is loss or impaired sense of smell and so many PWP experience that (usually before motor symptoms appear....this was true for us) I can't help but think that this may have implications for PD as well.

I continue to be amazed at the research of folks here on the forum, what an incredible group.
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