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In This Issue of JAMA Neurology |

In This Issue of JAMA Neurology FREE

JAMA Neurol. 2013;70(5):547-548. doi:10.1001/jamaneurol.2013.76.
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IMAGING CORTICAL DAMAGE AND DYSFUNCTION IN MULTIPLE SCLEROSIS

Filippi and coauthors summarize the features of multiple sclerosis–related cortical pathology and discuss findings from studies using both conventional and modern quantitative magnetic resonance–based techniques for the assessment of cortical damage and dysfunction in patients with multiple sclerosis.

RANDOMIZED CONTROLLED CLINICAL TRIAL OF “VIRTUAL HOUSE CALLS” FOR PARKINSON DISEASE

In a 7-month, 2-center, randomized controlled clinical trial, Dorsey and colleagues evaluate the feasibility, effectiveness, and economic benefits of using web-based videoconferencing (telemedicine) to provide specialty care to patients with Parkinson disease in their homes.

PARKIN DISEASE: A CLINICOPATHOLOGIC ENTITY?

Doherty et al investigated whether parkin -linked parkinsonism is a different clinicopathologic entity to Parkinson disease. Editorial perspective is provided by J. Eric Ahlskog, PhD, MD..

PROGNOSIS OF MILD COGNITIVE IMPAIRMENT IN EARLY PARKINSON DISEASE: THE NORWEGIAN PARKWEST STUDY

In a population-based cohort, Pedersen et al evaluated the incidence of mild cognitive impairment and its progression to dementia during a 3-year study in 182 patients with Parkinson disease. Editorial perspective is provided by Brian J. Copeland, MD and Mya C. Schiess, MD.

SLEEP QUALITY AND PRECLINICAL ALZHEIMER DISEASE

In a cross-sectional study, Ju et al test whether Aβ deposition in preclinical Alzheimer disease, prior to the appearance of cognitive impairment, is associated with changes in quality or quantity of sleep.

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Prevalence of amyloid deposition by sleep efficiency group. Participants were grouped by sleep efficiency, at cutoffs of less than 75% and more than 89% for poor and good sleep efficiency, respectively. The proportion in each group with abnormal β-amyloid 42 (Aβ42) level (≤500 pg/mL) decreases with better sleep efficiency. The group with worst sleep efficiency compared with best sleep efficiency had an odds ratio of 5.6 (95% CI, 0.965-32.5) of having amyloid deposition (P = .06).

CORRELATION OF SPECIFIC AMYLOID-Β OLIGOMERS WITH TAU IN CEREBROSPINAL FLUID FROM COGNITIVELY NORMAL OLDER ADULTS

Handoko and colleagues investigated 2 specific amyloid-β (Aβ) oligomers, Aβ trimers and Aβ*56, in human cerebrospinal fluid (CSF); evaluated the effects of aging and Alzheimer disease; and aimed to obtain support for the hypothesis that they may be pathogenic by determining their relationships to CSF tau.

RISK FACTORS FOR Β-AMYLOID DEPOSITION IN HEALTHY AGING: VASCULAR AND GENETIC EFFECTS

In a cross-sectional study, Rodrigue et al investigate risk factors for β-amyloid deposition in cognitively healthy middle-aged and older adults.

PROXIMAL DOMINANT HEREDITARY MOTOR AND SENSORY NEUROPATHY WITH PROXIMAL DOMINANCE ASSOCIATION WITH MUTATION IN TRK-FUSED GENE

Lee et al perform whole-exome sequencing to determine the relationship between hereditary motor and sensory neuropathy with proximal dominance and a mutation in the TRK-fused gene in a Korean family.

NEUROPATHOLOGIC BASIS OF AGE-ASSOCIATED BRAIN ATROPHY

Erten-Lyons et al examine the association between brain atrophy during life and neuropathology in an elderly population.

CENTRAL VEINS IN BRAIN LESIONS VISUALIZED WITH HIGH-FIELD MAGNETIC RESONANCE IMAGING: A PATHOLOGICALLY SPECIFIC DIAGNOSTIC BIOMARKER FOR INFLAMMATORY DEMYELINATION IN THE BRAIN

In a prospective longitudinal cohort study, Mistry and coauthors assess the diagnostic value of visualizing central veins in brain lesions with magnetic resonance imaging for patients with possible multiple sclerosis for which a diagnosis is uncertain.

MICROCYSTIC INNER NUCLEAR LAYER ABNORMALITIES AND NEUROMYELITIS OPTICA

Gelfand and colleagues conducted an observational, retrospective study to establish whether microcystic inner nuclear layer abnormalities occur in neuromyelitis optica.

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Prevalence of amyloid deposition by sleep efficiency group. Participants were grouped by sleep efficiency, at cutoffs of less than 75% and more than 89% for poor and good sleep efficiency, respectively. The proportion in each group with abnormal β-amyloid 42 (Aβ42) level (≤500 pg/mL) decreases with better sleep efficiency. The group with worst sleep efficiency compared with best sleep efficiency had an odds ratio of 5.6 (95% CI, 0.965-32.5) of having amyloid deposition (P = .06).

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