by Researchers at The University of Texas at Arlington have made breakthroughs in identifying and characterizing abnormal forms of the brain protein, amyloid beta, which is believed to be a key factor in the development of Alzheimer’s disease. Their findings have been published in two separate studies in Scientific Reports and Analytical and Bioanalytical Chemistry.
While most individuals develop some level of amyloid beta as they age, researchers believe that abnormal forms of the protein are the driving force behind the development of the disease.
The team at The University of Texas at Arlington has developed innovative methods to identify and characterize the various irregular forms of amyloid beta. This breakthrough will contribute significantly to understanding the exact causes of Alzheimer’s, which has remained elusive until now.
According to Daniel W. Armstrong, the lead author of both studies and the Welch Distinguished Professor of Chemistry and Biochemistry, aberrant forms of amyloid beta can disrupt brain chemistry, complicating the development of medications and immunotherapies to slow the progression of the disease. The research conducted by Armstrong’s team marks the first description of new methods for detecting and characterizing these aberrant forms of amyloid beta. This newfound knowledge brings us one step closer to halting the progression of this devastating disease.
One of the challenges in identifying abnormal forms of amyloid beta lies in the fact that they possess the same mass and amino acid sequence as normal forms of the protein. However, the study published in Scientific Reports revealed that the most effective approach to isolating amyloid beta from the brain is through a technique called immunoprecipitation. This method allows for the successful identification and examination of the abnormal forms of the protein, known as epimers and isomers.
The findings from the study in Analytical and Bioanalytical Chemistry demonstrated that the widely-used technique of liquid chromatography-mass spectrometry produces distinct signals for normal and aberrant forms of amyloid beta. This indicates that the current methods of identification and quantification are unreliable unless properly corrected. The study highlighted the importance of accurately distinguishing between the different forms of amyloid beta when developing treatments and medications for Alzheimer’s.
Currently, many Alzheimer’s medications utilize monoclonal antibodies that bind to amyloid beta proteins in order to remove them from the brain and slow the progression of dementia symptoms. However, this research suggests that these medications may not effectively bind to the abnormal versions of amyloid beta, potentially explaining why they are not always successful in slowing disease progression.
Daniel W. Armstrong emphasized the importance of these findings in furthering our understanding of Alzheimer’s disease and developing more effective treatments. These discoveries provide hope in our ongoing efforts to combat this debilitating disease and alleviate its devastating symptoms.
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1. Source: Coherent Market Insights, Public sources, Desk research
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