Breakthrough In Understanding Alzheimer's Disease

Breakthrough In Understanding Alzheimer's Disease
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.
Researchers 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. The research was published in the journal Science Advances.
 
Alzheimer's is the most common form of dementia globally, and is the fourth leading cause of death in individuals over the age of 65. The condition is classically associated with memory loss. However, other symptoms and warning signs include difficulty performing familiar tasks, problems with language such as forgetting phrases or words, and changes in mood, behaviour and personality.
 
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.
 
Unlike blood vessels anywhere else in the body, those in the brain have properties that strictly regulate what gets in and out of the delicate tissue - this is what is known as the blood-brain barrier (BBB). The BBB functions as a tightly regulated site of energy and metabolite exchange between the brain tissue and the bloodstream.
 
The researchers 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. They found that distinct components of the blood vessels termed tight junctions were altered in Alzheimer's disease. The research team believe 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.
 
"The concept of periodic clearance of brain amyloid-beta across the BBB could hold tremendous potential for Alzheimer's patients in the future. The next steps are to consider how this might be achieved. 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," the researchers said.
 
Based on material originally posted by Trinity College Dublin