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Your search keyword '"Tzourio, Christophe"' showing total 11 results
Start Over Author "Tzourio, Christophe" Journal annals of neurology
11 results on '"Tzourio, Christophe"'

2. Genome-Wide Association Studies of Cerebral White Matter Lesion Burden

Author

Fornage, Myriam, Debette, Stephanie, Bis, Joshua C., Schmidt, Helena, Ikram, Arfan M., Dufouil, Carole, Sigurdsson, Sigurdur, Lumley, Thomas, DeStefano, Anita L., Fazekas, Franz, Vrooman, Henri A., Shibata, Dean K., Maillard, Pauline, Zijdenbos, Alex, Smith, Albert V., Gudnason, Haukur, de Boer, Renske, Cushman, Mary, Mazoyer, Bernard, Heiss, Gerardo, Vernooij, Meike W., Enzinger, Christian, Glazer, Nicole L., Beiser, Alexa, Knopman, David S., Cavalieri, Margherita, Niessen, Wiro J., Harris, Tamara B., Petrovic, Katja, Lopez, Oscar L., Au, Rhoda, Lambert, Jean-Charles, Hofman, Albert, Gottesman, Rebecca F., Garcia, Melissa, Heckbert, Susan R., Atwood, Larry D., Catellier, Diane J., Uitterlinden, Andre G., Yang, Qiong, Smith, Nicholas L., Aspelund, Thor, Romero, Jose R., Rice, Kenneth, Taylor, Kent D., Nalls, Michael A., Rotter, Jerome I., Sharrett, Richey, van Duijn, Cornelia M., Amouyel, Philippe, Wolf, Philip A., Gudnason, Vilmundur, van der Lugt, Aad, Boerwinkle, Eric, Psaty, Bruce M., Seshadri, Sudha, Tzourio, Christophe, Breteler, Monique M. B., Mosley, Thomas H., Schmidt, Reinhold, Longstreth, W. T., DeCarli, Charles, and Launer, Lenore J.

Published
2011
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3. Professional exposure to pesticides and Parkinson disease

Author

Elbaz, Alexis, primary, Clavel, Jacqueline, additional, Rathouz, Paul J., additional, Moisan, Frédéric, additional, Galanaud, Jean‐Philippe, additional, Delemotte, Bernard, additional, Alpérovitch, Annick, additional, and Tzourio, Christophe, additional

Published
2009
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5. CYP2D6 polymorphism, pesticide exposure, and Parkinson's disease

Author

Elbaz, Alexis, primary, Levecque, Clotilde, additional, Clavel, Jacqueline, additional, Vidal, Jean‐Sébastien, additional, Richard, Florence, additional, Amouyel, Philippe, additional, Alpérovitch, Annick, additional, Chartier‐Harlin, Marie‐Christine, additional, and Tzourio, Christophe, additional

Published
2004
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10. Homocysteine, white matter hyperintensities, and cognition in healthy elderly people

Author

Dufouil, Carole, Alpérovitch, Annick, Ducros, Véronique, and Tzourio, Christophe

Abstract

Hyperhomocysteinemia is associated with an increased risk of vascular disease, and recent results suggest that it also could increase the risk of dementia. We examined the relationship between homocysteine and cognitive decline in 1,241 subjects aged 61 to 73 years, followed up over 4 years. Plasma homocysteine levels were determined in all participants as well as cardiovascular risk factors, apolipoprotein E genotype, plasma levels of folate, and vitamin B12. Cognitive performances were assessed repeatedly by using Mini-Mental State Examination, Trail Making Test, Digit Symbol Substitution Test, and Finger Tapping Test. At 2-year follow-up, 841 subjects underwent cerebral magnetic resonance imaging, and white matter hyperintensities were rated visually. Analyses were adjusted for all cardiovascular risk factors. Cross-sectional analyses showed that higher concentrations of homocysteine were significantly related to poorer performances at all neuropsychological tests. Longitudinal analyses confirmed this finding. The odds of cognitive decline was 2.8-fold (p < 0.05) higher in subjects with homocysteine levels above 15μmol/L compared with those with homocysteine levels below 10μmol/L. In participants who underwent magnetic resonance imaging, the relationship between homocysteine and cognition was unchanged after taking into account white matter hyperintensities suggesting that white matter hyperintensities do not mediate the association between homocysteine and cognition. Ann Neurol 2003;53:000–000

Published
2003
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11. Complex segregation analysis of Parkinson's disease: The Mayo Clinic Family Study

Author

Alexis Elbaz, Walter A. Rocca, J. Eric Ahlskog, James H. Bower, Demetrius M. Maraganore, Kari J. Strain, Daniel J. Schaid, Shannon K. McDonnell, Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic College of Medicine, Epidemiology, Departments of Health Sciences Research, Neuroépidémiologie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Neurology, and Tzourio, Christophe

Subjects
Proband, Gerontology, Male, Pediatrics, Cohort Studies, 0302 clinical medicine, MESH: Aged, 80 and over, Medicine, Age of Onset, MESH: Cohort Studies, MESH: Aged, Aged, 80 and over, 0303 health sciences, education.field_of_study, MESH: Middle Aged, MESH: Risk, Parkinsonism, Family aggregation, Parkinson Disease, Middle Aged, Penetrance, Pedigree, Neurology, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Female, Medical Record Linkage, MESH: Medical Record Linkage, Cohort study, Adult, Risk, medicine.medical_specialty, MESH: Pedigree, MESH: Age of Onset, Minnesota, Population, 03 medical and health sciences, MESH: United States, Humans, MESH: Patient Selection, Family, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], education, MESH: Family, 030304 developmental biology, Aged, MESH: Humans, Models, Statistical, business.industry, Patient Selection, MESH: Adult, MESH: Minnesota, Complex segregation analysis, medicine.disease, MESH: Male, United States, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Neurology (clinical), Age of onset, business, MESH: Female, 030217 neurology & neurosurgery, MESH: Models, Statistical, MESH: Parkinson Disease
Abstract

Objective To conduct complex segregation analyses of Parkinson's disease (PD). Methods Data on the familial aggregation of PD remain conflicting. We conducted a historical cohort study of 1,234 relatives of 162 patients with PD representative of people of Olmsted County, MN, and of 3,009 relatives of 411 patients with PD referred to the Mayo Clinic. Relatives were interviewed and screened for parkinsonism either directly or through a proxy, those who screened positive were examined, or a copy of their medical record was obtained to confirm the diagnosis. For subjects who resided in Olmsted County, additional information was obtained from the archives of the Olmsted County Historical Society and from a records-linkage system. Results Thirty-two relatives of population-based probands and 69 relatives of referral patients developed PD (101 in total). Combining population-based and referral samples, the model that best explained the familial clustering of PD overall was a major gene with additive effect on the penetrance. This model predicted an average decrease in age at onset of PD of approximately 18 years for each copy of the putative high-risk allele. The best fitting model for younger onset PD (age ≤ 59 years) was an autosomal recessive model. The best fitting models for older onset PD (age > 59 years) were a recessive or an additive model. Interpretation The familial aggregation of PD may be explained in part by a major gene with additive effect on the penetrance. Ann Neurol 2006;59:788–795

Published
2006

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