A recent study carried out by a team of researchers at Rice University in Houston, Texas has revealed that a relatively low-cost light therapy may help effectively eliminate amyloid beta proteins, which are precursors to dementia and Alzheimer's disease onset. It has long been established that beta amyloid accumulation results in the development of the cognitive disorders. However, the scientific community has observed that drug treatments designed to target these proteins have not shown relative efficacy so far.
Now, the research team has developed an optic probe that glows over 100 times more brightly when it detects the fine fibers or fibrils of amyloid beta proteins. The concentrated light then oxidizes the fibers in order to prevent them from accumulating in the brain and affecting the patients' memory. Likewise, the research team has identified a specific binding site for the harmful proteins, which in turn may provide a new avenue for drug treatment. The treatment could serve as a cheaper resource in disease treatment, the experts have reported in the journal Chem.
"There's an interest in finding medications that will quench the deleterious effects of amyloid beta aggregates. But to create drugs for these, we first need to know how drugs or molecules in general can bind and interact with these fibrils, and this was not well known. Now we have a better idea of what the molecule needs to interact with these fibrils. If we can modify complexes so they absorb red light, which is transparent to tissue, we might be able to perform these photochemical modifications in living animals, and maybe someday in humans," lead researcher Professor Angel Marti stated.
"While we cannot see the rhenium complex, we can find the oxidation, or footprint, it produces on the amyloid peptide. That oxidation only happens right next to the place where it binds. The real importance of this research is that it allows us to see with a high degree of certainty where molecules can interact with amyloid beta fibrils. We imagine it might be possible someday to prevent symptoms of Alzheimer's by targeting amyloid beta in the same way we treat cholesterol in people now to prevent cardiovascular disease," Professor Marti added.
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