A breakthrough in the study of Alzheimer’s disease was published by Irish scientists this past week in Science Advantages, an international research journal.
According to a report by the Irish Mirror, researchers discovered the mechanism which regulates the clearance of amyloid plaque that builds up in the brains of Alzheimer’s patients and, when coupled with other irregularities, result in the degeneration of motor skills and cognitive function associated with dementia.
The mechanism is part of the blood-brain barrier, a molecular-level function unique to the brain in which cells allow certain things to pass through their walls while blocking other things out.
In a normally functioning brain, the blood-brain barrier clears out plaque buildup. In Alzheimer’s patients, that clearing-out process is inhibited.
While researchers don’t know why the process is flawed in Alzheimer’s patients, The Irish Times reported this week, they are encouraged that their discovery can lead to further study and, hopefully, “new treatments” based on the protein-clearing blood-brain barrier mechanism.
The scientists believe ‘periodic clearance’ of the protein across the blood-brain barrier (BBB) could lead to new treatments.
Dr. Matthew Campbell, a research assistant at Ireland’s Trinity College Dublin, was quoted as saying that the findings highlight the importance of approaching Alzheimer’s from a molecular level.
Our recent findings have highlighted the importance of understanding diseases at the molecular level. The concept of periodic clearance of brain amyloid-beta across the BBB could hold tremendous potential for Alzheimer’s patients in the future.
The study used the brain tissue from patients who’d suffered through Alzheimer’s during their lifetime and then compared what they saw under the microscope with predictive models they created in their laboratories.
What they discovered were “tight junctions” that allowed the clearance of amyloid plaque in healthy brains, but these junctions were altered in the brains of Alzheimer’s patients.