Friday, October 16, 2015

Wine Can Fight Alzheimer's?

         

          What does it mean to be closer to finding the cure for diseases that no one has truly been able to understand?  Alzheimer’s disease (AD) and other non-inheritable dementias may not all have one specific cause or origin, yet they may all have certain pathways in common.  Many researchers have dedicated years of extensive research in an attempt to map out the neural circuitry of the brain.  Contrary to popular opinion, there is so little we really know when it comes to how the brain functions in relation to many diseases. 

          In correspondence to the same mission, much light has been recently shed on the study of neuroprotection in the brain and the underlying mechanisms behind the regulation of specific proteins. Dr. Michael Collins came to Loyola University Chicago on October 13, 2015 to speak about his research on ethanol preconditioning and brain neuroprotective signaling.  Moderate ethanol preconditioning (MEP) was applied to cultures of rat brains in order to study possible mechanisms that can provide neuroprotection to the brain.  About 20 to 30mM of ethanol seemed to cause neuroprotection by preventing the effects of neurotoxic proteins.

          The first part of this study focused on trying to understand the mechanisms that would lead to a neuroprotective state in the brain.  Specifically, MEP was seen to cause changes in NMDA receptor activity.  Any major increase or decrease in activity of this receptor was also seen to increase activity in PKC.  Upstream PKC activity corresponded to increased activity of another tyrosine phosphorylating enzyme, FAK.  Finally, this leads to increased activity in the antioxidant protein, peroxiredoxin 2 (Prx2), which corresponds to a neuroprotective state of the brain. 


          The second part of this study focused on taking this new information a step further and charting into the unknown.  Previous studies were seen to show a similar mechanism in terms of trans-reservatrol, the natural compound found in red wine.  Trans-reservatrol also increased activity of the Prx2 enzyme causing protection from beta amyloids.  It was found that 5 ɥM of this compound lead to neuroprotection.  Now, the big question was if one could synergize the preconditioning modalities combinatorially?  Combining 10 mM of ethanol and 5 ɥM reservatrol actually decreased death of neurons down to 10 percent! 

          It turns out that Dr. Collin’s study was not the only one interested in the neuroprotection made possible by trans-reservatrol.  In fact, just last year the Journal of Alzheimer’s Disease published a study that analyzed the protein, Sirtuin 1.  The activity of this protein increases with added amounts of reservatrol.  Dr. Porquet and researchers at the University of Barcelona fed a dietary supplementation amount of reservatrol for 10 months to a group of mice that were modified to develop Alzheimer’s disease.  According to Mercè Pallàs, researcher from the Research Group on Aging and Neurodegeneration of UB and the Centre for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), “Results showed that reservatrol ameliorated short-term memory and stopped the accumulation of senile plaques and the development of the tau protein, the two most important characteristics of the disease.”  Analysis of the Sirtuin pathway in terms of reservatrol emphasizes the importance reservatrol has on neuroprotection for the brain.  This study in combination with Dr. Collin’s research shows that understanding the different mechanisms and pathways which influence a single response is much more complex than originally predicted.  It also opens up uncharted territory in terms of explanations for different non-inheritable mental illnesses. 

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