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Small Cerebral Vascular Disease (MVP) is one of the most commonly badociated causes of age-related dementia and cerebrovascular accident. New research, conducted by the University of Edinburgh, may have finally discovered the mechanism by which MV causes brain damage, as well as a potential treatment to prevent damage, and possibly to even reverse the process.
up to 45 percent of cases of dementia, and the vast majority of older people are suspected of displaying some signs of the disease. One study remarkably found up to 95 percent of subjects aged between 60 and 90 displayed some sign of sheep vesicular disease when examined by MRI.
New research has examined the early pathological features of MV and found that dysfunction in endothelial cells are some of the first signs of degenerative disease progression. These are cells that line the small blood vessels in the brain and, in the early stages of MV, secrete a protein that interferes with the production of myelin, an essential compound for the protection of brain cells.
The hypothesis was that this endothelial cell dysfunction could be repaired, so subsequent brain damage from the MV could be avoided. The study was successful in treating rats treated with MV using drugs that stabilize this endothelial cell dysfunction. Not only have the symptoms of MV disappeared but, in the early stage of the disease, the treatment has reversed the badociated brain lesions.
"This important research helps us understand why small vessel disease occurs, providing a direct link between blood vessels and changes in the brain that are related to dementia," says the corresponding author of the Study, Anna Williams. "It also shows that these changes can be reversible, which opens the door to potential treatments."
These are still early stages of research, and these effects are only demonstrated in animal models, but this underlying endothelial dysfunction has been observed. human cases with early asymptomatic SVD. A big question about this discovery is whether the newly discovered treatment is directly correlated with a reversal of the clinical symptoms badociated with dementia or if, once these symptoms have taken root, too much damage has already been reversed. At least, the researchers hope that this study will help move toward a treatment that could offer an early or even preventative drug that limits the damaging degenerative effects of the MV. Considering the extremely prolific nature of MV in the elderly, and the current lack of any direct treatment, this research suggests promising avenues for future studies.
Source: University of Edinburgh
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