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In this issue (p 204) Cohn et al. show that excess TGF-β signaling is associated with myopathy in mouse models of Marfan syndrome and Duchenne muscular dystrophy. They further demonstrate that treatment with either antibodies to TGF-β or the heart medication losartan leads to normalization of muscle architecture and function in vivo. The cover depicts muscle, stained for nuclear DNA (blue), myosin (red) and laminin-λ 1 (green), displaying regeneration in the Duchenne mouse model treated with losartan. Image courtesy of Ronald Cohn and Harry Dietz.
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A drug commonly used to treat high blood pressure shows promise as a treatment in mouse models of Marfan syndrome and muscular dystrophy (pages 204–210).
An orally available drug enters the brain and interferes with signaling of orexin neuropeptides—providing a potential treatment for sleep disorders and possibly addiction (pages 150–155).
The nuclear hormone receptor LXR—best known for sensing cholesterol metabolites—also responds to glucose. The findings give LXR a central role in modulating the body's response to metabolic inputs.
The ability to visualize brain pathology in living individuals with Alzheimer disease could change how the disease is diagnosed and drugs to treat it tested. A recently developed positron emission tomography tracer helps to image fibrillar amyloid-β and neurofibrillary tangles and brings us closer to this goal.
A new approach to treating leaky blood vessels emerges from a proteomic analysis. The findings have implications for diabetic retinopathy and other diseases associated with increased vascular permeability (pages 181–188).
An inhibitor of the Wnt signaling pathway mediates bone destruction in inflammatory arthritis. The inhibitor may be the key to understanding why in some joint diseases bone is destroyed and in others built up (pages 156–163).