Month: January 2014
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Research reveals new therapeutic targets for Huntington’s and Parkinson’s disease
Research from Western University (London, Canada) has revealed a possible new target for treating movement disorders such as Huntington’s disease (HD) and Parkinson’s disease. Stephen Ferguson, PhD, a scientist at Western’s Robarts Research Institute, and Fabiola Ribeiro, PhD, of the Universidade Federal de Minas Gerais in Brazil found a definite improvement in motor behaviours in…
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How metabolism and brain activity are linked
Study sheds light on why diet may help control seizures in epilepsy patients A new study by scientists at McGill University and the University of Zurich shows a direct link between metabolism in brain cells and their ability to signal information. The research may explain why the seizures of many epilepsy patients can be controlled…
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Study conducted at Lady Davis Institute reveals new evidence that Caspase-6 is key to the cognitive impairment in Alzheimer’s disease
Through a series of studies, Dr. Andréa LeBlanc, a principal investigator at the Lady Davis Institute at the Jewish General Hospital, has discovered elevated levels of the protein Caspase-6 in the area of the brain – namely, the hippocampus, which is responsible for memory and cognition – first damaged by Alzheimer’s disease. This phenomenon is…
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Stopping tumours in their path
New study sheds light on most common and deadly form of brain cancer Glioblastoma (GBM) is the most common and deadly form of primary malignant brain cancer accounting for approximately 15% of all brain tumours and occurring mostly in adults between the ages of 45 and 70. The aggressive recurrent nature of this cancer is…
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Quality control of mitochondria as a defense against disease
Scientists from the Montreal Neurological Institute and Hospital in Canada have discovered that two genes linked to hereditary Parkinson’s disease are involved in the early-stage quality control of mitochondria. The protective mechanism, which is reported in The EMBO Journal, removes damaged proteins that arise from oxidative stress from mitochondria.