News Finding: Researchers say that further studies will need to test whether the treatment also works when the disease is firmly established.
Paper Finding: We identified a loss-of-function mutation in ATPase11B, which caused the EC dysfunction in the rat SVD model, and a singlenucleotide polymorphism in ATPase11B that was associated with white matter abnormalities in humans with SVD.
News Context: Treating rats with drugs that stop blood vessel cells from becoming dysfunctional reversed the symptoms of SVD and prevented brain damage, tests found. Researchers say that further studies will need to test whether the treatment also works when the disease is firmly established. They will also need to check if the treatment can reverse the symptoms of dementia.
Paper Context: EC and oligodendroglial dysfunction were also observed in humans with early, asymptomatic SVD pathology. We identified a loss-of-function mutation in ATPase11B, which caused the EC dysfunction in the rat SVD model, and a singlenucleotide polymorphism in ATPase11B that was associated with white matter abnormalities in humans with SVD. We show that EC dysfunction is a cause of SVD white matter vulnerability and provide a therapeutic strategy to treat and reverse SVD in the rat model, which may also be of relevance to human SVD.