Entity

Time filter

Source Type

Montreal, Canada

The Montreal Neurological Institute and Hospital is an academic medical centre dedicated to neuroscience research, training and clinical care. The institute is part of McGill University and the hospital is one of the six teaching hospitals of the McGill University Health Centre. They occupy separate sections of the same buildings on McGill's downtown Montreal campus next to Molson Stadium. The institute and hospital are locally known as "The Neuro." Wikipedia.


Trempe J.-F.,Montreal Neurological Institute
Current Opinion in Structural Biology | Year: 2011

Polyubiquitin chains are assembled through the formation of an isopeptide bond between a lysine side-chain or terminal amino group of a proximal ubiquitin moiety and the carboxy-terminal of a distal ubiquitin moiety. Protein substrates tagged by polyubiquitin chains of different linkages undergo different fates. Many polyubiquitin chain types have been characterized so far, notably Lys11, Lys48, Lys63 and linear chains. These different types of chains are synthesized, disassembled and recognized by selective enzymes and receptors. Here I survey the structural basis for the selective binding of polyubiquitin chains of specific linkages, with an emphasis on recent advances in our understanding of polyubiquitin chain structure and functions. Recent work suggests linkage-type discrimination by members of the NF-κb signalling and DNA repair pathways and a specific role for Lys48-linked polyubiquitin chain recognition by proteasome-associated proteins. © 2011 Elsevier Ltd. Source


Dagher A.,Montreal Neurological Institute
Trends in Endocrinology and Metabolism | Year: 2012

Obesity is a neurobehavioral disorder that results from a combination of overeating and insufficient physical activity. Finely tuned mechanisms exist to match food intake to caloric expenditure. However, faced with abundant inexpensive and calorie-dense foods, many humans (and perhaps most) have a tendency to consume beyond their caloric needs. The brain controls food intake by sensing internal energy-balance signals and external cues of food availability, and by controlling feeding behavior; it is therefore at the centre of the obesity problem. This article reviews the recent use of functional brain imaging in humans to study the neural control of appetite, and how the neural systems involved may cause vulnerability to overeating in the obesogenic environment. © 2012 Elsevier Ltd. Source


Sormani M.P.,University of Genoa | Arnold D.L.,Montreal Neurological Institute | De Stefano N.,University of Siena
Annals of Neurology | Year: 2014

Objective To evaluate the extent to which treatment effect on brain atrophy is able to mediate, at the trial level, the treatment effect on disability progression in relapsing-remitting multiple sclerosis (RRMS). Methods We collected all published randomized clinical trials in RRMS lasting at least 2 years and including as endpoints disability progression (defined as 6 or 3 months confirmed 1-point increase on the Expanded Disability Status Scale), active magnetic resonance imaging (MRI) lesions (defined as new/enlarging T2 lesions), and brain atrophy (defined as change in brain volume between month 24 and month 6-12). Treatment effects were expressed as relative reductions. A linear regression, weighted for trial size and duration, was used to assess the relationship between the treatment effects on MRI markers and on disability progression. Results Thirteen trials including >13,500 RRMS patients were included in the meta-analysis. Treatment effects on disability progression were correlated with treatment effects both on brain atrophy (R2 = 0.48, p = 0.001) and on active MRI lesions (R2 = 0.61, p < 0.001). When the effects on both MRI endpoints were included in a multivariate model, the correlation was higher (R2 = 0.75, p < 0.001), and both variables were retained as independently related to the treatment effect on disability progression. Interpretation In RRMS, the treatment effect on brain atrophy is correlated with the effect on disability progression over 2 years. This effect is independent of the effect of active MRI lesions on disability; the 2 MRI measures predict the treatment effect on disability more closely when used in combination. ANN NEUROL 2014;75:43-49 © 2014 American Neurological Association. Source


Perucca P.,Montreal Neurological Institute | Gilliam F.G.,Geisinger Health System
The Lancet Neurology | Year: 2012

More than 150 years after bromide was introduced as the first antiepileptic drug, adverse effects remain a leading cause of treatment failure and a major determinant of impaired health-related quality of life in people with epilepsy. Adverse effects can develop acutely or many years after starting treatment and can affect any organ or structure. In the past two decades, many efforts have been made to reduce the burden of antiepileptic drug toxicity. Several methods to screen and quantify adverse effects have been developed. Patient profiles associated with increased risk of specific adverse effects have been uncovered through advances in the areas of epidemiology and pharmacogenomics. Several new-generation antiepileptic drugs with improved tolerability profiles and reduced potential for drug interaction have been added to the therapeutic armamentarium. Overall, these advances have expanded the opportunities to tailor treatment with antiepileptic drugs, to enhance effectiveness and minimise the risk of toxic effects. © 2012 Elsevier Ltd. Source


La Piana R.,Montreal Neurological Institute
Archives of neurology | Year: 2012

To report a novel mutation in the gene EIF2B3 responsible for a late-onset form of vanishing white matter disease. Case report. University teaching hospital. A 29-year-old pregnant woman with a history of premature ovarian failure and hemiplegic migraines presented with a 10-week history of progressive confusion and headaches. Magnetic resonance imaging of the brain revealed a diffuse leukoencephalopathy. Sequencing of the exons and intron boundaries of EIF2B3 uncovered 2 missense mutations: c.260C>T(p.Ala87Val) and c.272G>A(p.Arg91His). To our knowledge,the latter missense mutation has never been previously reported. This is the second report of adult-onset vanishing white matter disease due to mutations in EIF2B3 and the first report of the c.272G>A (p.Arg91His) missense mutation. Source

Discover hidden collaborations