ArticleNeuromuscular disorders : NMD2015
Abnormalities in brain structure and biochemistry associated with mdx mice measured by in vivo MRI and high resolution localized (1)H MRS.
Article in Neuromuscular disorders : NMD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Phospho-mimic βIII-tubulin rescues microtubule and cardiac defects in Duchenne muscular dystrophy mice.Journal of molecular and cellular cardiology · 2026Article
- Understanding Duchenne muscular dystrophy-associated brain pathology.Disease models & mechanisms · 2025Review
- Neuronal hyperexcitability in dystrophin-deficient mdx hippocampal neurons: the importance of interleukin-6 and GABAergic regulation.Scientific reports · 2025Article
- Astrocyte proliferation in the hippocampal dentate gyrus is suppressed across the lifespan of dystrophin-deficient mdx mice.Experimental physiology · 2025Article
- Dmd mdx mice have defective oligodendrogenesis, delayed myelin compaction and persistent hypomyelination.Disease models & mechanisms · 2024Article
- Brain magnetic resonance imaging in the DE50-MD dog model of Duchenne muscular dystrophy reveals regional reductions in cerebral gray matter.BMC neuroscience · 2023Article
- Neural substrates of neuropsychological profiles in dystrophynopathies: A pilot study of diffusion tractography imaging.PloS one · 2021Article
- In Vivo Evaluation of White Matter Abnormalities in Children with Duchenne Muscular Dystrophy Using DTI.AJNR. American journal of neuroradiology · 2020Article
- Dystrophin Dp71 and the Neuropathophysiology of Duchenne Muscular Dystrophy.Molecular neurobiology · 2020Review
- Abnormalities in Brain and Muscle Microstructure and Neurochemistry of the DMD Rat Measured byFrontiers in neuroscience · 2020Article
- Advances in imaging of brain abnormalities in neuromuscular disease.Therapeutic advances in neurological disorders · 2019Review
- Visual Discrimination, Serial Reversal, and Extinction Learning in theFrontiers in behavioral neuroscience · 2019Article
- Influence of full-length dystrophin on brain volumes in mouse models of Duchenne muscular dystrophy.PloS one · 2018Article
- Myelination is delayed during postnatal brain development in the mdx mouse model of Duchenne muscular dystrophy.BMC neuroscience · 2017Article
- Cognitive dysfunction in Duchenne muscular dystrophy: a possible role for neuromodulatory immune molecules.Journal of neurophysiology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD), an X-linked disorder caused by the lack of dystrophin, is characterized by the progressive wasting of skeletal muscles. To date, what is known about dystrophin function is derived from studies of dystrophin-deficient animals, with the most common model being the mdx mouse. Most studies on patients with DMD and in mdx mice have focused on skeletal muscle and the development of therapies to reverse, or at least slow, the severe muscle wasting and progressive degeneration. However, dystrophin is also expressed in the CNS. Both mdx mice and patients with DMD can have cognitive and behavioral changes, but studies in the dystrophic brain are limited. We examined the brain structure and metabolites of mature wild type (WT) and mdx mice using magnetic resonance imaging and spectroscopy (MRI/MRS). Both structural and metabolic alterations were observed in the mdx brain. Enlarged lateral ventricles were detected in mdx mice when compared to WT. Diffusion tensor imaging (DTI) revealed elevations in diffusion diffusivities in the prefrontal cortex and a reduction of fractional anisotropy in the hippocampus. Metabolic changes included elevations in phosphocholine and glutathione, and a reduction in γ-aminobutyric acid in the hippocampus. In addition, an elevation in taurine was observed in the prefrontal cortex. Such findings indicate a regional structural change, altered cellular antioxidant defenses, a dysfunction of GABAergic neurotransmission, and a perturbed osmoregulation in the brain lacking dystrophin.
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