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In brief

Nature Reviews Neurology volume 6, page 470 (2010)Cite this article

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Gain-of-function mutations in KCNJ11, which encodes an ATP-sensitive potassium (KATP) channel subunit, cause neonatal diabetes. The origin of the motor impairments seen in patients with this condition has been unclear. A study now reveals that mice harboring a mutant allele of human KCNJ11 show motor deficits similar to those seen in neonatal diabetes, but only when the mutant subunit is expressed in CNS neurons. Thus, according to the researchers, therapies for such deficits should target neuronal rather than muscle KATP channels.

Patients with multiple sclerosis (MS) often exhibit cognitive deficits, which can be difficult to detect reliably. Lechner-Scott et al. compared the capabilities of the Audio Recorded Cognitive Screen (ARCS), a recently described 5 min cognitive assessment, and the more-established Paced Auditory Serial Addition Test (PASAT) to detect such deficits. In this study, 87 patients with MS completed both tests, with the investigators finding that the ARCS was more sensitive than the PASAT for the detection of impairment in any cognitive domain.

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ORIGINAL RESEARCH PAPERS

  1. Clark, R. H. et al. Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin. Science 329, 458–461 (2010)

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  2. Lechner-Scott, J. et al. The Audio Recorded Cognitive Screen (ARCS) in patients with multiple sclerosis: a practical tool for multiple sclerosis clinics. Mult. Scler. doi:101177/135245854743

  3. Petereit, H.-F. et al. Soluble CSF interleukin 2 receptor as indicators of neurosarcoidosis. J. Neurol. doi:10.1007/s00415-010-5623-3

  4. Berr, C. et al. Occupational exposure to solvents and cognitive performance in the GAZEL cohort: preliminary results. Dement. Geriatr. Cogn. Disord. 30, 12–19 (2010)

    Article  CAS  Google Scholar 

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In brief. Nat Rev Neurol 6, 470 (2010). https://doi.org/10.1038/nrneurol.2010.125

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