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Your search for author "Robert H. Brown" returned 32 results.

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  • Mutations in the vesicular trafficking protein annexin A11 are associated with amyotrophic lateral sclerosis

    Annexin A11 mutations, implicated in ALS, prevent binding to calcyclin and induce the formation of cytoplasmic inclusions.

  • Poly(GP) proteins are a useful pharmacodynamic marker for C9ORF72-associated amyotrophic lateral sclerosis

    Poly(GP) proteins are a promising pharmacodynamic marker for developing and testing therapeutics for treating C9ORF72-associated amyotrophic lateral sclerosis.

  • Endogenous retroviruses in ALS: A reawakening?

    New data incriminate the human endogenous retrovirus HERV-K in the pathogenesis of ALS and document that the HERV-K envelope protein can be neurotoxic (Li et al., this issue).

  • Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways

    Analysis of the expressed genes of nearly 2900 patients with amyotrophic lateral sclerosis and about 6400 controls reveals a disease predisposition–associated gene. [Also see Perspective by Singleton and Traynor]

  • Multimodal Actions of Neural Stem Cells in a Mouse Model of ALS: A Meta-Analysis

    A meta-analysis reports the beneficial effects of transplanting mouse or human neural stem cells into the spinal cord of the SOD1G93A mouse, a model of ALS.

  • dSarm/Sarm1 Is Required for Activation of an Injury-Induced Axon Death Pathway

    Mutations in a scaffold protein block the Wallerian degeneration of axons in flies and mice.

  • Targeting Nrf2 Signaling Improves Bacterial Clearance by Alveolar Macrophages in Patients with COPD and in a Mouse Model

    Bacterial clearance in macrophages from lungs with chronic obstructive pulmonary disease is improved by stimulating the Nrf2 antioxidant signaling pathway.

  • A Reinnervating MicroRNA

    A microRNA expressed in skeletal muscle promotes the regeneration of neuromuscular synapses after injury and in a neurodegenerative disease model.

  • Neuron Research Leaps Ahead

    Technologies that reprogram adult dermal cells into motor neurons should advance our understanding of neurodegenerative diseases.

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