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4 results

  • The Comprehensive Assessment of Neurodegeneration and Dementia: Canadian Cohort Study

  • Howard Chertkow, Michael Borrie, Victor Whitehead, Sandra E. Black, Howard H. Feldman, Serge Gauthier, David B. Hogan, Mario Masellis, Katherine McGilton, Kenneth Rockwood, Mary C. Tierney, Melissa Andrew, Ging-Yuek R. Hsiung, Richard Camicioli, Eric E. Smith, Jennifer Fogarty, Joseph Lindsay, Sarah Best, Alan Evans, Samir Das, Zia Mohaddes, Randi Pilon, Judes Poirier, Natalie A. Phillips, Elizabeth MacNamara, Roger A. Dixon, Simon Duchesne, Ian MacKenzie, R. Jane Rylett
  • Journal: Canadian Journal of Neurological Sciences / Volume 46 / Issue 5 / September 2019
  • Published online by Cambridge University Press: 16 July 2019, pp. 499-511
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  • Background:

    The Comprehensive Assessment of Neurodegeneration and Dementia (COMPASS-ND) cohort study of the Canadian Consortium on Neurodegeneration in Aging (CCNA) is a national initiative to catalyze research on dementia, set up to support the research agendas of CCNA teams. This cross-country longitudinal cohort of 2310 deeply phenotyped subjects with various forms of dementia and mild memory loss or concerns, along with cognitively intact elderly subjects, will test hypotheses generated by these teams.

    Methods:

    The COMPASS-ND protocol, initial grant proposal for funding, fifth semi-annual CCNA Progress Report submitted to the Canadian Institutes of Health Research December 2017, and other documents supplemented by modifications made and lessons learned after implementation were used by the authors to create the description of the study provided here.

    Results:

    The CCNA COMPASS-ND cohort includes participants from across Canada with various cognitive conditions associated with or at risk of neurodegenerative diseases. They will undergo a wide range of experimental, clinical, imaging, and genetic investigation to specifically address the causes, diagnosis, treatment, and prevention of these conditions in the aging population. Data derived from clinical and cognitive assessments, biospecimens, brain imaging, genetics, and brain donations will be used to test hypotheses generated by CCNA research teams and other Canadian researchers. The study is the most comprehensive and ambitious Canadian study of dementia. Initial data posting occurred in 2018, with the full cohort to be accrued by 2020.

    Conclusion:

    Availability of data from the COMPASS-ND study will provide a major stimulus for dementia research in Canada in the coming years.

  • Environment, Genetics and Idiopathic Parkinson's Disease

  • Judes Poirier, Sandra Kogan, Serge Gauthier
  • Journal: Canadian Journal of Neurological Sciences / Volume 18 / Issue 1 / February 1991
  • Published online by Cambridge University Press: 18 September 2015, pp. 70-76
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  • Since Idiopathic Parkinson's disease (IPD) was first described more than 170 years ago, there have been major advances in the understanding of the etiology of the disease as well as in its treatment. This article will review current knowledge concerning the role of the environment, genetic hypotheses and the aging factor in the etiology of IPD and proposes a complex interaction involving all these factors. Hypotheses regarding mitochondrial inhibition and free radical generation in IPD are discussed in relation to the mechanism of action of neurotoxins known to produce parkinsonian syndromes.

  • Altered Gene Expression in Alzheimer's Disease Brain Tissue

  • Patrick C. May, Steven A. Johnson, Judes Poirier, Martha Lampert-Etchells, Caleb E. Finch
  • Journal: Canadian Journal of Neurological Sciences / Volume 16 / Issue S4 / November 1989
  • Published online by Cambridge University Press: 18 September 2015, pp. 473-476
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  • We review the evidence for altered gene expression in Alzheimer's disease brain and identify alternative molecular approaches for isolating additional novel markers. One marker, pADHC-9, was isolated from a human hippocampal cDNA library by differential screening with AD and control cDNA probes. This clone hybridizes to a 2 Kb RNA which is increased 2 fold in AD hippocampus. The deduced amino acid sequence of pADHC-9 codes for a 52 kDAL protein similar to a testicular sulfated glycoprotein secreted by rat Sertoli cells. The normal function of this protein in brain and whether that function is altered in Alzheimer's disease is unknown.

  • 17 - Apolipoprotein E as a marker in the treatment of Alzheimer's disease

  • from Part V - Specific psychotropic drugs and disorders
  • Edited by Bernard Lerer, Hadassah-Hebrew Medical Center, Jerusalem
  • Book: Pharmacogenetics of Psychotropic Drugs
  • Published online: 20 August 2009
  • Print publication: 29 August 2002, pp 360-371

  • Summary

    This chapter focuses specifically on the pharmacogenetic role of the risk factor gene apolipoprotein E (ApoE) in Alzheimer's disease (AD) and in the response of patients with AD to treatment. ApoE has been extensively studied in non-nervous tissues as one of several proteins that regulate lipid transport and metabolism. ApoE facilitates cholesterol (and phospholipid) transport between different cell types and different organs. It binds to large lipid-protein particles (called lipoproteins). The chapter divides AD drug therapy into two broad categories, the cholinergic and noncholinergic drugs. One of the goals of pharmacogenetics is to deliver the right medicine to the right patient. The retrospective studies presented here show that the pharmacogenetic impact of the apoE alleles are a step in this direction as there are definitely drugs that work better in non-apoE4 carriers (for example, tacrine) and those that work better in the apoE4 carriers (for example, S12024).