[ad_1]
Researchers at the University of Virginia School of Medicine (United States) have discovered how and why A traumatic brain injury (TBI) increases the risk of Alzheimer’s, and their work suggests a possible way to prevent this increase.
The doctor John Lukensdirector of the UVA Harrison Family Translational Research Center in Alzheimer’s and Neurodegenerative Diseases, and his collaborators discovered that a single mild TBI causes detrimental changes in the brain that facilitate the onset of Alzheimer’s.
Furthermore, they managed to prevent these changes in laboratory mice by using a hollowed-out virus to deliver repair substances to the brain’s protective membranes.
“Our findings indicate that repairing brain drainage after head trauma may provide a much-needed strategy to limit the development of Alzheimer’s disease later in life,” he said. Lukensmember of the UVA Department of Neuroscience and its Center for Brain and Glial Immunology (BIG Center).
“We hope these discoveries inspire the design of new therapies.” that enhance brain drainage and that can be used to accelerate the recovery of the injured brain and limit the risk of developing Alzheimer’s,” he adds.
Traumatic brain injuries significantly increase the risk of Alzheimer’s and other neurodegenerative diseases, but scientists have had little understanding of why. Lukens’ new research suggests that such injuries impair the function of lymphatic vessels that connect the brain with the immune system.
These vessels, located in the meninges, protective membranes of the brain, were thought not to exist until they were discovered by UVA neuroscience researchers in 2015. It is now known that lVessels play a vital role in cleaning and protecting the brain.
The work of Lukens suggests that TBI accelerates the accumulation of the harmful tau protein associated with Alzheimer’s disease, and that these tau tangles are not necessarily confined to the site of injury. In laboratory mice, a single mild TBI worsened overall brain health and stimulated neurodegeneration.
Scientists were able to identify specific effects caused by mild TBI, including harmful changes in the activity of immune cells called macrophages which act as brain defenders and waste eliminators.
“This research reinforces our understanding of some of the devastating long-term consequences of brain injury and its relationship to neurodegenerative diseases,” says Dr. Ashley Boltedoctor of medicine from UVA and member of the research team. “Traumatic brain injury is a condition for which we currently have very few medical interventions, so a potential therapeutic target is very promising.”
In this way, scientists discovered that they could act on the 24 hours following an injury to protect the brain and restore the function of vital lymphatic vessels. They used a hollowed-out viral envelope to deliver a substance called VEGFC directly to the meninges.
This “lymphatic growth factor” occurs naturally in the body to promote vessel growth and repair, and its administration to the meninges prevented harmful tau production.
They note that much more research will be needed before this approach can be used as a treatment in people, but scientists say it holds great promise for preventing TBI-related neurodegeneration. This could help prevent not only Alzheimer’s, but also other neurological diseases, according to researchers.
“Traumatic brain injury has also been linked to other neurodegenerative disorders, such as ALS, Parkinson’s disease, and chronic traumatic encephalopathy (CTE),” Lukens said. “Exploring whether recovery of brain drainage after traumatic brain injury is also effective in protecting against these other devastating neurodegenerative diseases will be an important area of future research for our laboratory and others.”
[ad_2]
Source link
