A human donor Alzheimer’s disease brain tissue stained with an agent called ‘congo-red’, which allows for the visualization of amyloid-beta plaques (red) in the brain and surrounding blood vessels. Blue stains show the nuclei of the cells in the brain. Credit: Dr Matthew Campbell, 2015
Researchers believe that periodic clearance of a specific protein across the blood brain barrier could hold tremendous potential for new therapies. Scientists at Trinity College Dublin have shed light on a fundamental mechanism underlying the development of Alzheimer’s disease, which could lead to new forms of therapy for those living with the condition.
Alzheimer’s disease is characterized, in part, by the build-up of a small protein (‘amyloid-beta’) in the brains of patients. Impaired clearance of this protein appears to be a major factor in the build-up of plaques, and then in the disease process itself. While the mode by which amyloid-beta is cleared remains unclear, it is evident that it needs to be removed from the brain via the bloodstream.
“We have shown that distinct components of these blood vessels termed tight junctions are altered in Alzheimer’s disease. We think that this alteration could be an entrained mechanism to allow for the clearance of toxic amyloid-beta from the brain in those living with Alzheimer’s disease,” said postdoctoral researcher in Trinity’s School of Genetics and Microbiology, Dr James Keaney.
Working with the Dublin Brain Bank, Beaumont Hospital, the researchers from Trinity examined brain tissues of individuals who were affected by Alzheimer’s disease during their lifetime and then compared results to those observed in model systems in the laboratory. Dr Matthew Campbell, added: The results show involvement of the paracellular pathway in autoregulated Aβ movement across the BBB and identify both claudin-5 and occludin as potential therapeutic targets for AD. These findings also indicate that controlled modulation of tight junction components at the BBB can enhance the clearance of Aβ from the brain.
“Given the recent advances in clinical trials of anti-amyloid beta antibodies, we hope our findings may lead to improved and adjunctive forms of therapy for this devastating condition.” http://advances.sciencemag.org/content/1/8/e1500472 http://www.eurekalert.org/pub_releases/2015-09/tcd-trr091715.php
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