Author: "Clarke, Carl" / Publication Type: Electronic Resources - Searchworks@Jio Institute Digital Library Search Results

Your search keyword '"Clarke, Carl"' showing total 29 results

Start Over Author "Clarke, Carl" Publication Type Electronic Resources

29 results on '"Clarke, Carl"'

1. Investigation of Shared Genetic Risk Factors Between Parkinson's Disease and Cancers

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND Courage-PD [sponsor], Sugier, Pierre-Emmanuel, Lucotte, Elise A., Domenighetti, Cloé, Law, Matthew H., Iles, Mark M., Brown, Kevin, Amos, Christopher, McKay, James D., Hung, Rayjean J., Karimi, Mojgan, Bacq-Daian, Delphine, Boland-Augé, Anne, Olaso, Robert, Deleuze, Jean-François, Lesueur, Fabienne, Ostroumova, Evgenia, Kesminiene, Ausrele, de Vathaire, Florent, Guénel, Pascal, consortium, The Epithyr, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimios, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Nakayama, Akiyoshi, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy, Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Rödström, Emil Ygland, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Landoulsi, Zied, consortium, Courage-PD, Truong, Thérèse, Elbaz, Ales, Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND Courage-PD [sponsor], Sugier, Pierre-Emmanuel, Lucotte, Elise A., Domenighetti, Cloé, Law, Matthew H., Iles, Mark M., Brown, Kevin, Amos, Christopher, McKay, James D., Hung, Rayjean J., Karimi, Mojgan, Bacq-Daian, Delphine, Boland-Augé, Anne, Olaso, Robert, Deleuze, Jean-François, Lesueur, Fabienne, Ostroumova, Evgenia, Kesminiene, Ausrele, de Vathaire, Florent, Guénel, Pascal, consortium, The Epithyr, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimios, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Nakayama, Akiyoshi, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy, Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Rödström, Emil Ygland, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Landoulsi, Zied, consortium, Courage-PD, Truong, Thérèse, and Elbaz, Ales
Abstract: Background Epidemiological studies that examined the association between Parkinson's disease (PD) and cancers led to inconsistent results, but they face a number of methodological difficulties. Objective We used results from genome-wide association studies (GWASs) to study the genetic correlation between PD and different cancers to identify common genetic risk factors. Methods We used individual data for participants of European ancestry from the Courage-PD (Comprehensive Unbiased Risk Factor Assessment for Genetics and Environment in Parkinson's Disease; PD, N = 16,519) and EPITHYR (differentiated thyroid cancer, N = 3527) consortia and summary statistics of GWASs from iPDGC (International Parkinson Disease Genomics Consortium; PD, N = 482,730), Melanoma Meta-Analysis Consortium (MMAC), Breast Cancer Association Consortium (breast cancer), the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (prostate cancer), International Lung Cancer Consortium (lung cancer), and Ovarian Cancer Association Consortium (ovarian cancer) (N comprised between 36,017 and 228,951 for cancer GWASs). We estimated the genetic correlation between PD and cancers using linkage disequilibrium score regression. We studied the association between PD and polymorphisms associated with cancers, and vice versa, using cross-phenotypes polygenic risk score (PRS) analyses. Results We confirmed a previously reported positive genetic correlation of PD with melanoma (Gcorr = 0.16 [0.04; 0.28]) and reported an additional significant positive correlation of PD with prostate cancer (Gcorr = 0.11 [0.03; 0.19]). There was a significant inverse association between the PRS for ovarian cancer and PD (odds ratio [OR] = 0.89 [0.84; 0.94]). Conversely, the PRS of PD was positively associated with breast cancer (OR = 1.08 [1.06; 1.10]) and inversely associated with ovarian cancer (OR = 0.95 [0.91; 0.99]). The association between PD and ovarian cancer was mostly dri
Published: 2023

2. Dairy Intake and Parkinson's Disease: A Mendelian Randomization Study

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Fonds National de la Recherche - FnR [sponsor], JPND Courage-PD [sponsor], Domenighetti, Cloé, Sugier, Pierre-Emmanuel, Ashok Kumar Sreelatha, Ashwin, Schulte, Claudia, Grover, Sandeep, Mohamed, Océane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Correia Guedes, Leonor, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Genetics, The Comprehensive Unbiased Risk Factor Assessment For, Consortium, Environment In Parkinson S Disease Courage-P. D., Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Fonds National de la Recherche - FnR [sponsor], JPND Courage-PD [sponsor], Domenighetti, Cloé, Sugier, Pierre-Emmanuel, Ashok Kumar Sreelatha, Ashwin, Schulte, Claudia, Grover, Sandeep, Mohamed, Océane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Correia Guedes, Leonor, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Genetics, The Comprehensive Unbiased Risk Factor Assessment For, and Consortium, Environment In Parkinson S Disease Courage-P. D.
Abstract: Background Previous prospective studies highlighted dairy intake as a risk factor for Parkinson's disease (PD), particularly in men. It is unclear whether this association is causal or explained by reverse causation or confounding. Objective The aim is to examine the association between genetically predicted dairy intake and PD using two-sample Mendelian randomization (MR). Methods We genotyped a well-established instrumental variable for dairy intake located in the lactase gene (rs4988235) within the Courage-PD consortium (23 studies; 9823 patients and 8376 controls of European ancestry). Results Based on a dominant model, there was an association between genetic predisposition toward higher dairy intake and PD (odds ratio [OR] per one serving per day = 1.70, 95 confidence interval = 1.12–2.60, P = 0.013) that was restricted to men (OR = 2.50 [1.37–4.56], P = 0.003; P-difference with women = 0.029). Conclusions Using MR, our findings provide further support for a causal relationship between dairy intake and higher PD risk, not biased by confounding or reverse causation. Further studies are needed to elucidate the underlying mechanisms. © 2022 International Parkinson and Movement Disorder Society
Published: 2022

3. Dairy Intake and Parkinson's Disease: A Mendelian Randomization Study

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Fonds National de la Recherche - FnR [sponsor], JPND Courage-PD [sponsor], Domenighetti, Cloé, Sugier, Pierre-Emmanuel, Ashok Kumar Sreelatha, Ashwin, Schulte, Claudia, Grover, Sandeep, Mohamed, Océane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Correia Guedes, Leonor, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Genetics, The Comprehensive Unbiased Risk Factor Assessment For, Consortium, Environment In Parkinson S Disease Courage-P. D., Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Fonds National de la Recherche - FnR [sponsor], JPND Courage-PD [sponsor], Domenighetti, Cloé, Sugier, Pierre-Emmanuel, Ashok Kumar Sreelatha, Ashwin, Schulte, Claudia, Grover, Sandeep, Mohamed, Océane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaeva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Harlin, Marie-Christine, Mutez, Eugénie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotaka, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart P. C., Bloem, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrøm, Lasse, Correia Guedes, Leonor, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Fairen, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, Dimitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Genetics, The Comprehensive Unbiased Risk Factor Assessment For, and Consortium, Environment In Parkinson S Disease Courage-P. D.
Abstract: Background Previous prospective studies highlighted dairy intake as a risk factor for Parkinson's disease (PD), particularly in men. It is unclear whether this association is causal or explained by reverse causation or confounding. Objective The aim is to examine the association between genetically predicted dairy intake and PD using two-sample Mendelian randomization (MR). Methods We genotyped a well-established instrumental variable for dairy intake located in the lactase gene (rs4988235) within the Courage-PD consortium (23 studies; 9823 patients and 8376 controls of European ancestry). Results Based on a dominant model, there was an association between genetic predisposition toward higher dairy intake and PD (odds ratio [OR] per one serving per day = 1.70, 95 confidence interval = 1.12–2.60, P = 0.013) that was restricted to men (OR = 2.50 [1.37–4.56], P = 0.003; P-difference with women = 0.029). Conclusions Using MR, our findings provide further support for a causal relationship between dairy intake and higher PD risk, not biased by confounding or reverse causation. Further studies are needed to elucidate the underlying mechanisms. © 2022 International Parkinson and Movement Disorder Society
Published: 2022

4. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, and Elbaz, Alexis
Abstract: Background:Previous studies showed that lifestyle behaviors (cigarette smoking, alcohol, coffee) are inversely associated with Parkinson’s disease (PD). The prodromal phase of PD raises the possibility that these associations may be explained by reverse causation. Objective:To examine associations of lifestyle behaviors with PD using two-sample Mendelian randomisation (MR) and the potential for survival and incidence-prevalence biases. Methods:We used summary statistics from publicly available studies to estimate the association of genetic polymorphisms with lifestyle behaviors, and from Courage-PD (7,369 cases, 7,018 controls; European ancestry) to estimate the association of these variants with PD. We used the inverse-variance weighted method to compute odds ratios (ORIVW) of PD and 95%confidence intervals (CI). Significance was determined using a Bonferroni-corrected significance threshold (p = 0.017). Results:We found a significant inverse association between smoking initiation and PD (ORIVW per 1-SD increase in the prevalence of ever smoking = 0.74, 95%CI = 0.60–0.93, p = 0.009) without significant directional pleiotropy. Associations in participants ≤67 years old and cases with disease duration ≤7 years were of a similar size. No significant associations were observed for alcohol and coffee drinking. In reverse MR, genetic liability toward PD was not associated with smoking or coffee drinking but was positively associated with alcohol drinking. Conclusion:Our findings are in favor of an inverse association between smoking and PD that is not explained by reverse causation, confounding, and survival or incidence-prevalence biases. Genetic liability toward PD was positively associated with alcohol drinking. Conclusions on the association of alcohol and coffee drinking with PD are hampered by insufficient statistical power.
Published: 2021

5. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, and Elbaz, Alexis
Abstract: Background:Previous studies showed that lifestyle behaviors (cigarette smoking, alcohol, coffee) are inversely associated with Parkinson’s disease (PD). The prodromal phase of PD raises the possibility that these associations may be explained by reverse causation. Objective:To examine associations of lifestyle behaviors with PD using two-sample Mendelian randomisation (MR) and the potential for survival and incidence-prevalence biases. Methods:We used summary statistics from publicly available studies to estimate the association of genetic polymorphisms with lifestyle behaviors, and from Courage-PD (7,369 cases, 7,018 controls; European ancestry) to estimate the association of these variants with PD. We used the inverse-variance weighted method to compute odds ratios (ORIVW) of PD and 95%confidence intervals (CI). Significance was determined using a Bonferroni-corrected significance threshold (p = 0.017). Results:We found a significant inverse association between smoking initiation and PD (ORIVW per 1-SD increase in the prevalence of ever smoking = 0.74, 95%CI = 0.60–0.93, p = 0.009) without significant directional pleiotropy. Associations in participants ≤67 years old and cases with disease duration ≤7 years were of a similar size. No significant associations were observed for alcohol and coffee drinking. In reverse MR, genetic liability toward PD was not associated with smoking or coffee drinking but was positively associated with alcohol drinking. Conclusion:Our findings are in favor of an inverse association between smoking and PD that is not explained by reverse causation, confounding, and survival or incidence-prevalence biases. Genetic liability toward PD was positively associated with alcohol drinking. Conclusions on the association of alcohol and coffee drinking with PD are hampered by insufficient statistical power.
Published: 2021

6. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, Elbaz, Alexis, Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], JPND [sponsor], Domenighetti, Cloe, Sugier, Pierre Emmanuel, Sreelatha, Ashwin Ashok Kumar, Schulte, Claudia, Grover, Sandeep, Mohamed, Oceane, Portugal, Berta, May, Patrick, Bobbili, Dheeraj Reddy, Radivojkov-Blagojevic, Milena, Lichtner, Peter, Singleton, Andrew B., Hernandez, Dena G., Edsall, Connor, Mellick, George D., Zimprich, Alexander, Pirker, Walter, Rogaieva, Ekaterina, Lang, Anthony E., Koks, Sulev, Taba, Pille, Lesage, Suzanne, Brice, Alexis, Corvol, Jean-Christophe, Chartier-Hardin, Marie-Christophe, Mutez, Eugenie, Brockmann, Kathrin, Deutschländer, Angela B., Hadjigeorgiou, Georges M., Dardiotis, Efthimos, Stefanis, Leonidas, Simitsi, Athina Maria, Valente, Enza-Maria, Petrucci, Simona, Duga, Stefano, Straniero, Letizia, Zecchinelli, Anna, Pezzoli, Gianni, Brighina, Laura, Ferrarese, Carlo, Annesi, Grazia, Quattrone, Andrea, Gagliardi, Monica, Matsuo, Hirotak, Kawamura, Yusuke, Hattori, Nobutaka, Nishioka, Kenya, Chung, Sun Ju, Kim, Yun Joong, Kolber, Pierre, van de Warrenburg, Bart Pc, Bloom, Bastiaan R., Aasly, Jan, Toft, Mathias, Pihlstrom, Lasse, Guedes, Leonor Correia, Ferreira, Joaquim J., Bardien, Soraya, Carr, Jonathan, Tolosa, Eduardo, Ezquerra, Mario, Pastor, Pau, Diez-Farien, Monica, Wirdefeldt, Karin, Pedersen, Nancy L., Ran, Caroline, Belin, Andrea C., Puschmann, Andreas, Hellberg, Clara, Clarke, Carl E., Morrison, Karen E., Tan, Manuela, Krainc, DImitri, Burbulla, Lena F., Farrer, Matt J., Krüger, Rejko, Gasser, Thomas, Sharma, Manu, and Elbaz, Alexis
Abstract: Background:Previous studies showed that lifestyle behaviors (cigarette smoking, alcohol, coffee) are inversely associated with Parkinson’s disease (PD). The prodromal phase of PD raises the possibility that these associations may be explained by reverse causation. Objective:To examine associations of lifestyle behaviors with PD using two-sample Mendelian randomisation (MR) and the potential for survival and incidence-prevalence biases. Methods:We used summary statistics from publicly available studies to estimate the association of genetic polymorphisms with lifestyle behaviors, and from Courage-PD (7,369 cases, 7,018 controls; European ancestry) to estimate the association of these variants with PD. We used the inverse-variance weighted method to compute odds ratios (ORIVW) of PD and 95%confidence intervals (CI). Significance was determined using a Bonferroni-corrected significance threshold (p = 0.017). Results:We found a significant inverse association between smoking initiation and PD (ORIVW per 1-SD increase in the prevalence of ever smoking = 0.74, 95%CI = 0.60–0.93, p = 0.009) without significant directional pleiotropy. Associations in participants ≤67 years old and cases with disease duration ≤7 years were of a similar size. No significant associations were observed for alcohol and coffee drinking. In reverse MR, genetic liability toward PD was not associated with smoking or coffee drinking but was positively associated with alcohol drinking. Conclusion:Our findings are in favor of an inverse association between smoking and PD that is not explained by reverse causation, confounding, and survival or incidence-prevalence biases. Genetic liability toward PD was positively associated with alcohol drinking. Conclusions on the association of alcohol and coffee drinking with PD are hampered by insufficient statistical power.
Published: 2021

7. The Genetic Architecture of Parkinson Disease in Spain: Characterizing Population-Specific Risk, Differential Haplotype Structures, and Providing Etiologic Insight

Author: National Institutes of Health (US), Department of Defense (US), Michael J. Fox Foundation for Parkinson's Research, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), European Commission, Junta de Andalucía, Sociedad Andaluza de Neurología, Jacques and Gloria Gossweiler Foundation, Fundación Alicia Koplowitz, Fundación Mutua Madrileña, Universidad de Sevilla, Bandres-Ciga, Sara, Ahmed, Sarah, Sabir, Marya S., Blauwendraat, Cornelis, Adarmes Gómez, A. D., Bernal-Bernal, Inmaculada, Bonilla-Toribio, Marta, Buiza-Rueda, Dolores, Carrillo, Fátima, Carrión-Claro, Mario, Gómez-Garre, Pilar, Jesús Maestre, Silvia, Labrador, Miguel Ángel, Macías García, Daniel, Méndez-Del Barrio, Carlota, Periñán, María Teresa, Tejera-Parrado, Cristina, Vargas-González, Laura, Díez-Fairen, Mónica, Álvarez, Ignacio, Tartari, J. P., Buongiorno, Maria Teresa, Aguilar, Miquel, Gorostidi, Ana, Bergareche, Jesús Alberto, Mondragon, Elisabet, Vinagre-Aragon, Ana, Croitoru, Ioana, Ruiz-Martínez, Javier, Dols-Icardo, Oriol, Kulisevsky, Jaime, Marín-Lahoz, Juan, Pagonabarraga-Mora, Javier, Pascual-Sedano, Berta, Ezquerra, Mario, Cámara, Ana, Compta, Yaroslau, Fernández Ortiga, Manel, Fernández-Santiago, Rubén, Muñoz, Esteban, Tolosa, Eduardo, Valldeoriola, Francesc, González-Aramburu, Isabel, Sanchez Rodriguez, Antonio, Sierra, María, Menéndez González, M., Blazquez, Marta, Garcia, Ciara, Suarez-San Martin, Esther, García-Ruíz, Pedro, Martínez-Castrillo, J. C., Vela-Desojo, Lydia, Ruz, Clara, Barrero, Francisco Javier, Escamilla-Sevilla, Francisco, Mínguez-Castellanos, Adolfo, Cerdan, Debora, Tabernero, César, Gomez Heredia, Maria Jose, Perez Errazquin, Francisco, Romero-Acebal, Manolo, Feliz, Cici, López-Sendón, José Luis, Mata, Marina, Martínez Torres, Irene, Kim, Jonggeol Jeffrey, Dalgard, Clifton L., Brooks, Janet, Saez-Atienzar, Sara, Gibbs, J. Raphael, Jorda, Rafael, Botia, Juan A., Bonet-Ponce, Luis, Morrison, Karen E., Clarke, Carl, Tan, Manuela, Morris, Huw, Edsall, Connor, Hernández, Dena, Simón-Sánchez, Javier, Nalls, Michael A., Scholz, Sonja, Jiménez Escrig, Adriano, Duarte, Jacinto, Vives, Francisco, Duran, Raquel, Hoenicka, Janet, Álvarez, Victoria, Infante, Jon, Martí, María-José, Clarimón, Jordi, López de Munain, Adolfo, Pastor, Pau, Mir, Pablo, Singleton, Andrew B., National Institutes of Health (US), Department of Defense (US), Michael J. Fox Foundation for Parkinson's Research, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), European Commission, Junta de Andalucía, Sociedad Andaluza de Neurología, Jacques and Gloria Gossweiler Foundation, Fundación Alicia Koplowitz, Fundación Mutua Madrileña, Universidad de Sevilla, Bandres-Ciga, Sara, Ahmed, Sarah, Sabir, Marya S., Blauwendraat, Cornelis, Adarmes Gómez, A. D., Bernal-Bernal, Inmaculada, Bonilla-Toribio, Marta, Buiza-Rueda, Dolores, Carrillo, Fátima, Carrión-Claro, Mario, Gómez-Garre, Pilar, Jesús Maestre, Silvia, Labrador, Miguel Ángel, Macías García, Daniel, Méndez-Del Barrio, Carlota, Periñán, María Teresa, Tejera-Parrado, Cristina, Vargas-González, Laura, Díez-Fairen, Mónica, Álvarez, Ignacio, Tartari, J. P., Buongiorno, Maria Teresa, Aguilar, Miquel, Gorostidi, Ana, Bergareche, Jesús Alberto, Mondragon, Elisabet, Vinagre-Aragon, Ana, Croitoru, Ioana, Ruiz-Martínez, Javier, Dols-Icardo, Oriol, Kulisevsky, Jaime, Marín-Lahoz, Juan, Pagonabarraga-Mora, Javier, Pascual-Sedano, Berta, Ezquerra, Mario, Cámara, Ana, Compta, Yaroslau, Fernández Ortiga, Manel, Fernández-Santiago, Rubén, Muñoz, Esteban, Tolosa, Eduardo, Valldeoriola, Francesc, González-Aramburu, Isabel, Sanchez Rodriguez, Antonio, Sierra, María, Menéndez González, M., Blazquez, Marta, Garcia, Ciara, Suarez-San Martin, Esther, García-Ruíz, Pedro, Martínez-Castrillo, J. C., Vela-Desojo, Lydia, Ruz, Clara, Barrero, Francisco Javier, Escamilla-Sevilla, Francisco, Mínguez-Castellanos, Adolfo, Cerdan, Debora, Tabernero, César, Gomez Heredia, Maria Jose, Perez Errazquin, Francisco, Romero-Acebal, Manolo, Feliz, Cici, López-Sendón, José Luis, Mata, Marina, Martínez Torres, Irene, Kim, Jonggeol Jeffrey, Dalgard, Clifton L., Brooks, Janet, Saez-Atienzar, Sara, Gibbs, J. Raphael, Jorda, Rafael, Botia, Juan A., Bonet-Ponce, Luis, Morrison, Karen E., Clarke, Carl, Tan, Manuela, Morris, Huw, Edsall, Connor, Hernández, Dena, Simón-Sánchez, Javier, Nalls, Michael A., Scholz, Sonja, Jiménez Escrig, Adriano, Duarte, Jacinto, Vives, Francisco, Duran, Raquel, Hoenicka, Janet, Álvarez, Victoria, Infante, Jon, Martí, María-José, Clarimón, Jordi, López de Munain, Adolfo, Pastor, Pau, Mir, Pablo, and Singleton, Andrew B.
Abstract: Background: The Iberian Peninsula stands out as having variable levels of population admixture and isolation, making Spain an interesting setting for studying the genetic architecture of neurodegenerative diseases. Objectives: To perform the largest PD genome-wide association study restricted to a single country. Methods: We performed a GWAS for both risk of PD and age at onset in 7,849 Spanish individuals. Further analyses included population-specific risk haplotype assessments, polygenic risk scoring through machine learning, Mendelian randomization of expression, and methylation data to gain insight into disease-associated loci, heritability estimates, genetic correlations, and burden analyses. Results: We identified a novel population-specific genome-wide association study signal at PARK2 associated with age at onset, which was likely dependent on the c.155delA mutation. We replicated four genome-wide independent signals associated with PD risk, including SNCA, LRRK2, KANSL1/MAPT, and HLA-DQB1. A significant trend for smaller risk haplotypes at known loci was found compared to similar studies of non-Spanish origin. Seventeen PD-related genes showed functional consequence by two-sample Mendelian randomization in expression and methylation data sets. Long runs of homozygosity at 28 known genes/loci were found to be enriched in cases versus controls. Conclusions: Our data demonstrate the utility of the Spanish risk haplotype substructure for future fine-mapping efforts, showing how leveraging unique and diverse population histories can benefit genetic studies of complex diseases. The present study points to PARK2 as a major hallmark of PD etiology in Spain.
Published: 2019

8. Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study.

Author: Wang, Lisa, Heckman, Michael G., Aasly, Jan O., Annesi, Grazia, Bozi, Maria, Chung, Sun Ju, Clarke, Carl, Crosiers, David, Eckstein, Gertrud, Garraux, Gaetan, Hadjigeorgiou, Georgios M., Hattori, Nobu, Jeon, Beom, Kim, Yun J., Kubo, Masato, Lesage, Suzanne, Lin, Juei Jueng, Lynch, Timothy, Lichtner, Peter, Mellick, George D., Mok, Vincent, Morrison, Karin E., Quattrone, Aldo, Satake, Wataru, Silburn, Peter A., Stefanis, Leonidas, Stockton, Joanne D., Tan, Eng King, Toda, Tatsushi, Brice, Alexis, Van Broeckhoven, Christine, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Maraganore, Demetrius M., Gasser, Thomas, Krüger, Rejko, Farrer, Matthew J., Ross, Owen A., Sharma, Manu, Wang, Lisa, Heckman, Michael G., Aasly, Jan O., Annesi, Grazia, Bozi, Maria, Chung, Sun Ju, Clarke, Carl, Crosiers, David, Eckstein, Gertrud, Garraux, Gaetan, Hadjigeorgiou, Georgios M., Hattori, Nobu, Jeon, Beom, Kim, Yun J., Kubo, Masato, Lesage, Suzanne, Lin, Juei Jueng, Lynch, Timothy, Lichtner, Peter, Mellick, George D., Mok, Vincent, Morrison, Karin E., Quattrone, Aldo, Satake, Wataru, Silburn, Peter A., Stefanis, Leonidas, Stockton, Joanne D., Tan, Eng King, Toda, Tatsushi, Brice, Alexis, Van Broeckhoven, Christine, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Maraganore, Demetrius M., Gasser, Thomas, Krüger, Rejko, Farrer, Matthew J., Ross, Owen A., and Sharma, Manu
Abstract: A recent study MacLeod et al. has shown that an interaction between variants at the LRRK2 and PARK16 loci influences risk of development of Parkinson's disease (PD). Our study examines the proposed interaction between LRRK2 and PARK16 variants in modifying PD risk using a large multicenter series of PD patients (7715) and controls (8261) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Our data does not support a strong direct interaction between LRRK2 and PARK16 variants; however, given the role of retromer and lysosomal pathways in PD, further studies are warranted.
Published: 2017
Full Text: View/download PDF

9. Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study.

Author: Wang, Lisa, Heckman, Michael G., Aasly, Jan O., Annesi, Grazia, Bozi, Maria, Chung, Sun Ju, Clarke, Carl, Crosiers, David, Eckstein, Gertrud, Garraux, Gaetan, Hadjigeorgiou, Georgios M., Hattori, Nobu, Jeon, Beom, Kim, Yun J., Kubo, Masato, Lesage, Suzanne, Lin, Juei Jueng, Lynch, Timothy, Lichtner, Peter, Mellick, George D., Mok, Vincent, Morrison, Karin E., Quattrone, Aldo, Satake, Wataru, Silburn, Peter A., Stefanis, Leonidas, Stockton, Joanne D., Tan, Eng King, Toda, Tatsushi, Brice, Alexis, Van Broeckhoven, Christine, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Maraganore, Demetrius M., Gasser, Thomas, Krüger, Rejko, Farrer, Matthew J., Ross, Owen A., Sharma, Manu, Wang, Lisa, Heckman, Michael G., Aasly, Jan O., Annesi, Grazia, Bozi, Maria, Chung, Sun Ju, Clarke, Carl, Crosiers, David, Eckstein, Gertrud, Garraux, Gaetan, Hadjigeorgiou, Georgios M., Hattori, Nobu, Jeon, Beom, Kim, Yun J., Kubo, Masato, Lesage, Suzanne, Lin, Juei Jueng, Lynch, Timothy, Lichtner, Peter, Mellick, George D., Mok, Vincent, Morrison, Karin E., Quattrone, Aldo, Satake, Wataru, Silburn, Peter A., Stefanis, Leonidas, Stockton, Joanne D., Tan, Eng King, Toda, Tatsushi, Brice, Alexis, Van Broeckhoven, Christine, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Maraganore, Demetrius M., Gasser, Thomas, Krüger, Rejko, Farrer, Matthew J., Ross, Owen A., and Sharma, Manu
Abstract: A recent study MacLeod et al. has shown that an interaction between variants at the LRRK2 and PARK16 loci influences risk of development of Parkinson's disease (PD). Our study examines the proposed interaction between LRRK2 and PARK16 variants in modifying PD risk using a large multicenter series of PD patients (7715) and controls (8261) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Our data does not support a strong direct interaction between LRRK2 and PARK16 variants; however, given the role of retromer and lysosomal pathways in PD, further studies are warranted.
Published: 2017
Full Text: View/download PDF

10. Large-scale replication and heterogeneity in Parkinson disease genetic loci.

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Van Broeckhoven, Christine, Bertram, Lars, Bozi, Maria, Crosiers, David, Clarke, Carl, Facheris, Maurizio, Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, Krüger, Rejko, Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Van Broeckhoven, Christine, Bertram, Lars, Bozi, Maria, Crosiers, David, Clarke, Carl, Facheris, Maurizio, Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, and Krüger, Rejko
Abstract: OBJECTIVE: Eleven genetic loci have reached genome-wide significance in a recent meta-analysis of genome-wide association studies in Parkinson disease (PD) based on populations of Caucasian descent. The extent to which these genetic effects are consistent across different populations is unknown. METHODS: Investigators from the Genetic Epidemiology of Parkinson's Disease Consortium were invited to participate in the study. A total of 11 SNPs were genotyped in 8,750 cases and 8,955 controls. Fixed as well as random effects models were used to provide the summary risk estimates for these variants. We evaluated between-study heterogeneity and heterogeneity between populations of different ancestry. RESULTS: In the overall analysis, single nucleotide polymorphisms (SNPs) in 9 loci showed significant associations with protective per-allele odds ratios of 0.78-0.87 (LAMP3, BST1, and MAPT) and susceptibility per-allele odds ratios of 1.14-1.43 (STK39, GAK, SNCA, LRRK2, SYT11, and HIP1R). For 5 of the 9 replicated SNPs there was nominally significant between-site heterogeneity in the effect sizes (I(2) estimates ranged from 39% to 48%). Subgroup analysis by ethnicity showed significantly stronger effects for the BST1 (rs11724635) in Asian vs Caucasian populations and similar effects for SNCA, LRRK2, LAMP3, HIP1R, and STK39 in Asian and Caucasian populations, while MAPT rs2942168 and SYT11 rs34372695 were monomorphic in the Asian population, highlighting the role of population-specific heterogeneity in PD. CONCLUSION: Our study allows insight to understand the distribution of newly identified genetic factors contributing to PD and shows that large-scale evaluation in diverse populations is important to understand the role of population-specific heterogeneity.
Published: 2012
Full Text: View/download PDF

11. A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants.

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Bertram, Lars, Bozi, Maria, Barcikowska, Maria, Crosiers, David, Clarke, Carl E., Facheris, Maurizio F., Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom S., Jamrozik, Zygmunt, Krygowska-Wajs, Anna, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Libioulle, Cecile, Murata, Miho, Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Meitnger, Thomas, Zimprich, Alexander, Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Strom, Tim M., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Van Broeckhoven, Christine, Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yomono, Harumi S., Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, Krüger, Rejko, Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Bertram, Lars, Bozi, Maria, Barcikowska, Maria, Crosiers, David, Clarke, Carl E., Facheris, Maurizio F., Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom S., Jamrozik, Zygmunt, Krygowska-Wajs, Anna, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Libioulle, Cecile, Murata, Miho, Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Meitnger, Thomas, Zimprich, Alexander, Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Strom, Tim M., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Van Broeckhoven, Christine, Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yomono, Harumi S., Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, and Krüger, Rejko
Abstract: BACKGROUND: Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease . Although additional missense variants were described, their pathogenic role yet remains inconclusive. METHODS AND RESULTS: We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any significant increased risk for p.Leu774Met and p.Gly51Ser in our cohort. CONCLUSIONS: Our study apart from identifying the p.Asp620Asn variant in familial cases also identified it in idiopathic Parkinson disease cases, and thus provides genetic evidence for a role of p.Asp620Asn in Parkinson disease in different populations worldwide.
Published: 2012
Full Text: View/download PDF

12. A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants.

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Bertram, Lars, Bozi, Maria, Barcikowska, Maria, Crosiers, David, Clarke, Carl E., Facheris, Maurizio F., Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom S., Jamrozik, Zygmunt, Krygowska-Wajs, Anna, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Libioulle, Cecile, Murata, Miho, Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Meitnger, Thomas, Zimprich, Alexander, Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Strom, Tim M., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Van Broeckhoven, Christine, Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yomono, Harumi S., Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, Krüger, Rejko, Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Bertram, Lars, Bozi, Maria, Barcikowska, Maria, Crosiers, David, Clarke, Carl E., Facheris, Maurizio F., Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom S., Jamrozik, Zygmunt, Krygowska-Wajs, Anna, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Libioulle, Cecile, Murata, Miho, Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Meitnger, Thomas, Zimprich, Alexander, Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Strom, Tim M., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Van Broeckhoven, Christine, Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yomono, Harumi S., Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, and Krüger, Rejko
Abstract: BACKGROUND: Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease . Although additional missense variants were described, their pathogenic role yet remains inconclusive. METHODS AND RESULTS: We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any significant increased risk for p.Leu774Met and p.Gly51Ser in our cohort. CONCLUSIONS: Our study apart from identifying the p.Asp620Asn variant in familial cases also identified it in idiopathic Parkinson disease cases, and thus provides genetic evidence for a role of p.Asp620Asn in Parkinson disease in different populations worldwide.
Published: 2012
Full Text: View/download PDF

13. Large-scale replication and heterogeneity in Parkinson disease genetic loci.

Author: Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Van Broeckhoven, Christine, Bertram, Lars, Bozi, Maria, Crosiers, David, Clarke, Carl, Facheris, Maurizio, Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, Krüger, Rejko, Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) [research center], Sharma, Manu, Ioannidis, John P. A., Aasly, Jan O., Annesi, Grazia, Brice, Alexis, Van Broeckhoven, Christine, Bertram, Lars, Bozi, Maria, Crosiers, David, Clarke, Carl, Facheris, Maurizio, Farrer, Matthew, Garraux, Gaetan, Gispert, Suzana, Auburger, Georg, Vilarino-Guell, Carles, Hadjigeorgiou, Georgios M., Hicks, Andrew A., Hattori, Nobutaka, Jeon, Beom, Lesage, Suzanne, Lill, Christina M., Lin, Juei-Jueng, Lynch, Timothy, Lichtner, Peter, Lang, Anthony E., Mok, Vincent, Jasinska-Myga, Barbara, Mellick, George D., Morrison, Karen E., Opala, Grzegorz, Pramstaller, Peter P., Pichler, Irene, Park, Sung Sup, Quattrone, Aldo, Rogaeva, Ekaterina, Ross, Owen A., Stefanis, Leonidas, Stockton, Joanne D., Satake, Wataru, Silburn, Peter A., Theuns, Jessie, Tan, Eng-King, Toda, Tatsushi, Tomiyama, Hiroyuki, Uitti, Ryan J., Wirdefeldt, Karin, Wszolek, Zbigniew, Xiromerisiou, Georgia, Yueh, Kuo-Chu, Zhao, Yi, Gasser, Thomas, Maraganore, Demetrius, and Krüger, Rejko
Abstract: OBJECTIVE: Eleven genetic loci have reached genome-wide significance in a recent meta-analysis of genome-wide association studies in Parkinson disease (PD) based on populations of Caucasian descent. The extent to which these genetic effects are consistent across different populations is unknown. METHODS: Investigators from the Genetic Epidemiology of Parkinson's Disease Consortium were invited to participate in the study. A total of 11 SNPs were genotyped in 8,750 cases and 8,955 controls. Fixed as well as random effects models were used to provide the summary risk estimates for these variants. We evaluated between-study heterogeneity and heterogeneity between populations of different ancestry. RESULTS: In the overall analysis, single nucleotide polymorphisms (SNPs) in 9 loci showed significant associations with protective per-allele odds ratios of 0.78-0.87 (LAMP3, BST1, and MAPT) and susceptibility per-allele odds ratios of 1.14-1.43 (STK39, GAK, SNCA, LRRK2, SYT11, and HIP1R). For 5 of the 9 replicated SNPs there was nominally significant between-site heterogeneity in the effect sizes (I(2) estimates ranged from 39% to 48%). Subgroup analysis by ethnicity showed significantly stronger effects for the BST1 (rs11724635) in Asian vs Caucasian populations and similar effects for SNCA, LRRK2, LAMP3, HIP1R, and STK39 in Asian and Caucasian populations, while MAPT rs2942168 and SYT11 rs34372695 were monomorphic in the Asian population, highlighting the role of population-specific heterogeneity in PD. CONCLUSION: Our study allows insight to understand the distribution of newly identified genetic factors contributing to PD and shows that large-scale evaluation in diverse populations is important to understand the role of population-specific heterogeneity.
Published: 2012
Full Text: View/download PDF

14. AN ANALYSIS OF THE DETERMINANTS OF DEMAND FOR TOURISM IN BARBADOS.

Author: CLARKE, CARL DENZIL and CLARKE, CARL DENZIL
Abstract: not available
Published: 1978

15. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

Author: Clarke, Carl E., Walker, Marion F., Sackley, Catherine M., Clarke, Carl E., Walker, Marion F., and Sackley, Catherine M.
Full Text: View/download PDF

16. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, Sackley, Catherine M., Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, and Sackley, Catherine M.
Abstract: Background Cochrane reviews of physiotherapy (PT) and occupational therapy (OT) for Parkinson’s disease found insufficient evidence of effectiveness, but previous trials were methodologically flawed with small sample size and short-term follow-up. Objectives To evaluate the clinical effectiveness and cost-effectiveness of individualised PT and OT in Parkinson’s disease. Design Large pragmatic randomised controlled trial. Setting Thirty-eight neurology and geriatric medicine outpatient clinics in the UK. Participants Seven hundred and sixty-two patients with mild to moderate Parkinson’s disease reporting limitations in activities of daily living (ADL). Intervention Patients were randomised online to either both PT and OT NHS services (n = 381) or no therapy (n = 381). Therapy incorporated a patient-centred approach with individual assessment and goal setting. Main outcome measures The primary outcome was instrumental ADL measured by the patient-completed Nottingham Extended Activities of Daily Living (NEADL) scale at 3 months after randomisation. Secondary outcomes were health-related quality of life [Parkinson’s Disease Questionnaire-39 (PDQ-39); European Quality of Life-5 Dimensions (EQ-5D)], adverse events, resource use and carer quality of life (Short Form questionnaire-12 items). Outcomes were assessed before randomisation and at 3, 9 and 15 months after randomisation. Results Data from 92% of the participants in each group were available at the primary time point of 3 months, but there was no difference in NEADL total score [difference 0.5 points, 95% confidence interval (CI) –0.7 to 1.7; p = 0.4] or PDQ-39 summary index (0.007 points, 95% CI –1.5 to 1.5; p = 1.0) between groups. The EQ-5D quotient was of borderline significance in favour of therapy (–0.03, 95% CI –0.07 to –0.002; p = 0.04). Contact time with therapists was for a median of four visits of 58 minutes each over 8 weeks (mean dose 232 minutes). Repeated measures analysis including all time points s
Full Text: View/download PDF

17. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Sackley, Catherine Mary, Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., and Sackley, Catherine Mary
Abstract: IMPORTANCE It is unclear whether physiotherapy and occupational therapy are clinically effective and cost-effective in Parkinson disease (PD). OBJECTIVE To perform a large pragmatic randomized clinical trial to evaluate the clinical effectiveness of individualized physiotherapy and occupational therapy in PD. DESIGN, SETTING, AND PARTICIPANTS The PD REHAB Trial was a multicenter, open-label, parallel group, controlled efficacy trial. A total of 762 patients with mild to moderate PD were recruited from 38 sites across the United Kingdom. Recruitment took place between October 2009 and June 2012, with 15 months of follow-up. INTERVENTIONS Participants with limitations in activities of daily living (ADL) were randomized to physiotherapy and occupational therapy or no therapy. MAIN OUTCOMES AND MEASURES The primary outcome was the Nottingham Extended Activities of Daily Living (NEADL) Scale score at 3 months after randomization. Secondary outcomes were health-related quality of life (assessed by Parkinson Disease Questionnaire–39 and EuroQol-5D); adverse events; and caregiver quality of life. Outcomes were assessed before trial entry and then 3, 9, and 15 months after randomization. RESULTS Of the 762 patients included in the study (mean [SD] age, 70 [9.1] years), 381 received physiotherapy and occupational therapy and 381 received no therapy. At 3 months, there was no difference between groups in NEADL total score (difference, 0.5 points; 95%CI, −0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire–39 summary index (0.007 points; 95%CI, −1.5 to 1.5; P = .99). The EuroQol-5D quotient was of borderline significance in favor of therapy (−0.03; 95%CI, −0.07 to −0.002; P = .04). The median therapist contact time was 4 visits of 58 minutes over 8 weeks. Repeated-measures analysis showed no difference in NEADL total score, but Parkinson Disease Questionnaire–39 summary index (diverging 1.6 points per annum; 95%CI, 0.47 to 2.62; P = .005) and EuroQol-5D score (0.02; 95%CI
Full Text: View/download PDF

18. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Sackley, Catherine Mary, Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., and Sackley, Catherine Mary
Abstract: IMPORTANCE It is unclear whether physiotherapy and occupational therapy are clinically effective and cost-effective in Parkinson disease (PD). OBJECTIVE To perform a large pragmatic randomized clinical trial to evaluate the clinical effectiveness of individualized physiotherapy and occupational therapy in PD. DESIGN, SETTING, AND PARTICIPANTS The PD REHAB Trial was a multicenter, open-label, parallel group, controlled efficacy trial. A total of 762 patients with mild to moderate PD were recruited from 38 sites across the United Kingdom. Recruitment took place between October 2009 and June 2012, with 15 months of follow-up. INTERVENTIONS Participants with limitations in activities of daily living (ADL) were randomized to physiotherapy and occupational therapy or no therapy. MAIN OUTCOMES AND MEASURES The primary outcome was the Nottingham Extended Activities of Daily Living (NEADL) Scale score at 3 months after randomization. Secondary outcomes were health-related quality of life (assessed by Parkinson Disease Questionnaire–39 and EuroQol-5D); adverse events; and caregiver quality of life. Outcomes were assessed before trial entry and then 3, 9, and 15 months after randomization. RESULTS Of the 762 patients included in the study (mean [SD] age, 70 [9.1] years), 381 received physiotherapy and occupational therapy and 381 received no therapy. At 3 months, there was no difference between groups in NEADL total score (difference, 0.5 points; 95%CI, −0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire–39 summary index (0.007 points; 95%CI, −1.5 to 1.5; P = .99). The EuroQol-5D quotient was of borderline significance in favor of therapy (−0.03; 95%CI, −0.07 to −0.002; P = .04). The median therapist contact time was 4 visits of 58 minutes over 8 weeks. Repeated-measures analysis showed no difference in NEADL total score, but Parkinson Disease Questionnaire–39 summary index (diverging 1.6 points per annum; 95%CI, 0.47 to 2.62; P = .005) and EuroQol-5D score (0.02; 95%CI
Full Text: View/download PDF

19. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, Sackley, Catherine M., Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, and Sackley, Catherine M.
Abstract: Background Cochrane reviews of physiotherapy (PT) and occupational therapy (OT) for Parkinson’s disease found insufficient evidence of effectiveness, but previous trials were methodologically flawed with small sample size and short-term follow-up. Objectives To evaluate the clinical effectiveness and cost-effectiveness of individualised PT and OT in Parkinson’s disease. Design Large pragmatic randomised controlled trial. Setting Thirty-eight neurology and geriatric medicine outpatient clinics in the UK. Participants Seven hundred and sixty-two patients with mild to moderate Parkinson’s disease reporting limitations in activities of daily living (ADL). Intervention Patients were randomised online to either both PT and OT NHS services (n = 381) or no therapy (n = 381). Therapy incorporated a patient-centred approach with individual assessment and goal setting. Main outcome measures The primary outcome was instrumental ADL measured by the patient-completed Nottingham Extended Activities of Daily Living (NEADL) scale at 3 months after randomisation. Secondary outcomes were health-related quality of life [Parkinson’s Disease Questionnaire-39 (PDQ-39); European Quality of Life-5 Dimensions (EQ-5D)], adverse events, resource use and carer quality of life (Short Form questionnaire-12 items). Outcomes were assessed before randomisation and at 3, 9 and 15 months after randomisation. Results Data from 92% of the participants in each group were available at the primary time point of 3 months, but there was no difference in NEADL total score [difference 0.5 points, 95% confidence interval (CI) –0.7 to 1.7; p = 0.4] or PDQ-39 summary index (0.007 points, 95% CI –1.5 to 1.5; p = 1.0) between groups. The EQ-5D quotient was of borderline significance in favour of therapy (–0.03, 95% CI –0.07 to –0.002; p = 0.04). Contact time with therapists was for a median of four visits of 58 minutes each over 8 weeks (mean dose 232 minutes). Repeated measures analysis including all time points s
Full Text: View/download PDF

20. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

Author: Clarke, Carl E., Walker, Marion F., Sackley, Catherine M., Clarke, Carl E., Walker, Marion F., and Sackley, Catherine M.
Full Text: View/download PDF

21. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, Sackley, Catherine M., Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, and Sackley, Catherine M.
Abstract: Background Cochrane reviews of physiotherapy (PT) and occupational therapy (OT) for Parkinson’s disease found insufficient evidence of effectiveness, but previous trials were methodologically flawed with small sample size and short-term follow-up. Objectives To evaluate the clinical effectiveness and cost-effectiveness of individualised PT and OT in Parkinson’s disease. Design Large pragmatic randomised controlled trial. Setting Thirty-eight neurology and geriatric medicine outpatient clinics in the UK. Participants Seven hundred and sixty-two patients with mild to moderate Parkinson’s disease reporting limitations in activities of daily living (ADL). Intervention Patients were randomised online to either both PT and OT NHS services (n = 381) or no therapy (n = 381). Therapy incorporated a patient-centred approach with individual assessment and goal setting. Main outcome measures The primary outcome was instrumental ADL measured by the patient-completed Nottingham Extended Activities of Daily Living (NEADL) scale at 3 months after randomisation. Secondary outcomes were health-related quality of life [Parkinson’s Disease Questionnaire-39 (PDQ-39); European Quality of Life-5 Dimensions (EQ-5D)], adverse events, resource use and carer quality of life (Short Form questionnaire-12 items). Outcomes were assessed before randomisation and at 3, 9 and 15 months after randomisation. Results Data from 92% of the participants in each group were available at the primary time point of 3 months, but there was no difference in NEADL total score [difference 0.5 points, 95% confidence interval (CI) –0.7 to 1.7; p = 0.4] or PDQ-39 summary index (0.007 points, 95% CI –1.5 to 1.5; p = 1.0) between groups. The EQ-5D quotient was of borderline significance in favour of therapy (–0.03, 95% CI –0.07 to –0.002; p = 0.04). Contact time with therapists was for a median of four visits of 58 minutes each over 8 weeks (mean dose 232 minutes). Repeated measures analysis including all time points s
Full Text: View/download PDF

22. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

Author: Clarke, Carl E., Walker, Marion F., Sackley, Catherine M., Clarke, Carl E., Walker, Marion F., and Sackley, Catherine M.
Full Text: View/download PDF

23. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Sackley, Catherine Mary, Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., and Sackley, Catherine Mary
Abstract: IMPORTANCE It is unclear whether physiotherapy and occupational therapy are clinically effective and cost-effective in Parkinson disease (PD). OBJECTIVE To perform a large pragmatic randomized clinical trial to evaluate the clinical effectiveness of individualized physiotherapy and occupational therapy in PD. DESIGN, SETTING, AND PARTICIPANTS The PD REHAB Trial was a multicenter, open-label, parallel group, controlled efficacy trial. A total of 762 patients with mild to moderate PD were recruited from 38 sites across the United Kingdom. Recruitment took place between October 2009 and June 2012, with 15 months of follow-up. INTERVENTIONS Participants with limitations in activities of daily living (ADL) were randomized to physiotherapy and occupational therapy or no therapy. MAIN OUTCOMES AND MEASURES The primary outcome was the Nottingham Extended Activities of Daily Living (NEADL) Scale score at 3 months after randomization. Secondary outcomes were health-related quality of life (assessed by Parkinson Disease Questionnaire–39 and EuroQol-5D); adverse events; and caregiver quality of life. Outcomes were assessed before trial entry and then 3, 9, and 15 months after randomization. RESULTS Of the 762 patients included in the study (mean [SD] age, 70 [9.1] years), 381 received physiotherapy and occupational therapy and 381 received no therapy. At 3 months, there was no difference between groups in NEADL total score (difference, 0.5 points; 95%CI, −0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire–39 summary index (0.007 points; 95%CI, −1.5 to 1.5; P = .99). The EuroQol-5D quotient was of borderline significance in favor of therapy (−0.03; 95%CI, −0.07 to −0.002; P = .04). The median therapist contact time was 4 visits of 58 minutes over 8 weeks. Repeated-measures analysis showed no difference in NEADL total score, but Parkinson Disease Questionnaire–39 summary index (diverging 1.6 points per annum; 95%CI, 0.47 to 2.62; P = .005) and EuroQol-5D score (0.02; 95%CI
Full Text: View/download PDF

24. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, Sackley, Catherine M., Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, and Sackley, Catherine M.
Abstract: Background Cochrane reviews of physiotherapy (PT) and occupational therapy (OT) for Parkinson’s disease found insufficient evidence of effectiveness, but previous trials were methodologically flawed with small sample size and short-term follow-up. Objectives To evaluate the clinical effectiveness and cost-effectiveness of individualised PT and OT in Parkinson’s disease. Design Large pragmatic randomised controlled trial. Setting Thirty-eight neurology and geriatric medicine outpatient clinics in the UK. Participants Seven hundred and sixty-two patients with mild to moderate Parkinson’s disease reporting limitations in activities of daily living (ADL). Intervention Patients were randomised online to either both PT and OT NHS services (n = 381) or no therapy (n = 381). Therapy incorporated a patient-centred approach with individual assessment and goal setting. Main outcome measures The primary outcome was instrumental ADL measured by the patient-completed Nottingham Extended Activities of Daily Living (NEADL) scale at 3 months after randomisation. Secondary outcomes were health-related quality of life [Parkinson’s Disease Questionnaire-39 (PDQ-39); European Quality of Life-5 Dimensions (EQ-5D)], adverse events, resource use and carer quality of life (Short Form questionnaire-12 items). Outcomes were assessed before randomisation and at 3, 9 and 15 months after randomisation. Results Data from 92% of the participants in each group were available at the primary time point of 3 months, but there was no difference in NEADL total score [difference 0.5 points, 95% confidence interval (CI) –0.7 to 1.7; p = 0.4] or PDQ-39 summary index (0.007 points, 95% CI –1.5 to 1.5; p = 1.0) between groups. The EQ-5D quotient was of borderline significance in favour of therapy (–0.03, 95% CI –0.07 to –0.002; p = 0.04). Contact time with therapists was for a median of four visits of 58 minutes each over 8 weeks (mean dose 232 minutes). Repeated measures analysis including all time points s
Full Text: View/download PDF

25. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Sackley, Catherine Mary, Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., and Sackley, Catherine Mary
Abstract: IMPORTANCE It is unclear whether physiotherapy and occupational therapy are clinically effective and cost-effective in Parkinson disease (PD). OBJECTIVE To perform a large pragmatic randomized clinical trial to evaluate the clinical effectiveness of individualized physiotherapy and occupational therapy in PD. DESIGN, SETTING, AND PARTICIPANTS The PD REHAB Trial was a multicenter, open-label, parallel group, controlled efficacy trial. A total of 762 patients with mild to moderate PD were recruited from 38 sites across the United Kingdom. Recruitment took place between October 2009 and June 2012, with 15 months of follow-up. INTERVENTIONS Participants with limitations in activities of daily living (ADL) were randomized to physiotherapy and occupational therapy or no therapy. MAIN OUTCOMES AND MEASURES The primary outcome was the Nottingham Extended Activities of Daily Living (NEADL) Scale score at 3 months after randomization. Secondary outcomes were health-related quality of life (assessed by Parkinson Disease Questionnaire–39 and EuroQol-5D); adverse events; and caregiver quality of life. Outcomes were assessed before trial entry and then 3, 9, and 15 months after randomization. RESULTS Of the 762 patients included in the study (mean [SD] age, 70 [9.1] years), 381 received physiotherapy and occupational therapy and 381 received no therapy. At 3 months, there was no difference between groups in NEADL total score (difference, 0.5 points; 95%CI, −0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire–39 summary index (0.007 points; 95%CI, −1.5 to 1.5; P = .99). The EuroQol-5D quotient was of borderline significance in favor of therapy (−0.03; 95%CI, −0.07 to −0.002; P = .04). The median therapist contact time was 4 visits of 58 minutes over 8 weeks. Repeated-measures analysis showed no difference in NEADL total score, but Parkinson Disease Questionnaire–39 summary index (diverging 1.6 points per annum; 95%CI, 0.47 to 2.62; P = .005) and EuroQol-5D score (0.02; 95%CI
Full Text: View/download PDF

26. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

Author: Clarke, Carl E., Walker, Marion F., Sackley, Catherine M., Clarke, Carl E., Walker, Marion F., and Sackley, Catherine M.
Full Text: View/download PDF

27. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

Author: Clarke, Carl E., Walker, Marion F., Sackley, Catherine M., Clarke, Carl E., Walker, Marion F., and Sackley, Catherine M.
Full Text: View/download PDF

28. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Sackley, Catherine Mary, Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Dowling, Francis, Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., and Sackley, Catherine Mary
Abstract: IMPORTANCE It is unclear whether physiotherapy and occupational therapy are clinically effective and cost-effective in Parkinson disease (PD). OBJECTIVE To perform a large pragmatic randomized clinical trial to evaluate the clinical effectiveness of individualized physiotherapy and occupational therapy in PD. DESIGN, SETTING, AND PARTICIPANTS The PD REHAB Trial was a multicenter, open-label, parallel group, controlled efficacy trial. A total of 762 patients with mild to moderate PD were recruited from 38 sites across the United Kingdom. Recruitment took place between October 2009 and June 2012, with 15 months of follow-up. INTERVENTIONS Participants with limitations in activities of daily living (ADL) were randomized to physiotherapy and occupational therapy or no therapy. MAIN OUTCOMES AND MEASURES The primary outcome was the Nottingham Extended Activities of Daily Living (NEADL) Scale score at 3 months after randomization. Secondary outcomes were health-related quality of life (assessed by Parkinson Disease Questionnaire–39 and EuroQol-5D); adverse events; and caregiver quality of life. Outcomes were assessed before trial entry and then 3, 9, and 15 months after randomization. RESULTS Of the 762 patients included in the study (mean [SD] age, 70 [9.1] years), 381 received physiotherapy and occupational therapy and 381 received no therapy. At 3 months, there was no difference between groups in NEADL total score (difference, 0.5 points; 95%CI, −0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire–39 summary index (0.007 points; 95%CI, −1.5 to 1.5; P = .99). The EuroQol-5D quotient was of borderline significance in favor of therapy (−0.03; 95%CI, −0.07 to −0.002; P = .04). The median therapist contact time was 4 visits of 58 minutes over 8 weeks. Repeated-measures analysis showed no difference in NEADL total score, but Parkinson Disease Questionnaire–39 summary index (diverging 1.6 points per annum; 95%CI, 0.47 to 2.62; P = .005) and EuroQol-5D score (0.02; 95%CI
Full Text: View/download PDF

29. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Author: Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, Sackley, Catherine M., Clarke, Carl E., Patel, Smitaa, Ives, Natalie, Rick, Caroline E., Woolley, Rebecca, Wheatley, Keith, Walker, Marion F., Zhu, Shihua, Kandiyali, Rebecca, Yao, Guiqing, and Sackley, Catherine M.
Abstract: Background Cochrane reviews of physiotherapy (PT) and occupational therapy (OT) for Parkinson’s disease found insufficient evidence of effectiveness, but previous trials were methodologically flawed with small sample size and short-term follow-up. Objectives To evaluate the clinical effectiveness and cost-effectiveness of individualised PT and OT in Parkinson’s disease. Design Large pragmatic randomised controlled trial. Setting Thirty-eight neurology and geriatric medicine outpatient clinics in the UK. Participants Seven hundred and sixty-two patients with mild to moderate Parkinson’s disease reporting limitations in activities of daily living (ADL). Intervention Patients were randomised online to either both PT and OT NHS services (n = 381) or no therapy (n = 381). Therapy incorporated a patient-centred approach with individual assessment and goal setting. Main outcome measures The primary outcome was instrumental ADL measured by the patient-completed Nottingham Extended Activities of Daily Living (NEADL) scale at 3 months after randomisation. Secondary outcomes were health-related quality of life [Parkinson’s Disease Questionnaire-39 (PDQ-39); European Quality of Life-5 Dimensions (EQ-5D)], adverse events, resource use and carer quality of life (Short Form questionnaire-12 items). Outcomes were assessed before randomisation and at 3, 9 and 15 months after randomisation. Results Data from 92% of the participants in each group were available at the primary time point of 3 months, but there was no difference in NEADL total score [difference 0.5 points, 95% confidence interval (CI) –0.7 to 1.7; p = 0.4] or PDQ-39 summary index (0.007 points, 95% CI –1.5 to 1.5; p = 1.0) between groups. The EQ-5D quotient was of borderline significance in favour of therapy (–0.03, 95% CI –0.07 to –0.002; p = 0.04). Contact time with therapists was for a median of four visits of 58 minutes each over 8 weeks (mean dose 232 minutes). Repeated measures analysis including all time points s
Full Text: View/download PDF

Catalog

Books, media, physical & digital resources

See catalog results

Searchworks

Select search scope, currently: Articles

Catalog

books, media & more in Jio Institute collections

Articles

journal articles & other e-resources

Refine your results

29 results on '"Clarke, Carl"'

1. Investigation of Shared Genetic Risk Factors Between Parkinson's Disease and Cancers

2. Dairy Intake and Parkinson's Disease: A Mendelian Randomization Study

3. Dairy Intake and Parkinson's Disease: A Mendelian Randomization Study

4. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

5. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

6. Mendelian randomization study of smoking, alcohol, and coffee drinking in relation to Parkinso's disease

7. The Genetic Architecture of Parkinson Disease in Spain: Characterizing Population-Specific Risk, Differential Haplotype Structures, and Providing Etiologic Insight

8. Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study.

9. Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study.

10. Large-scale replication and heterogeneity in Parkinson disease genetic loci.

11. A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants.

12. A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants.

13. Large-scale replication and heterogeneity in Parkinson disease genetic loci.

14. AN ANALYSIS OF THE DETERMINANTS OF DEMAND FOR TOURISM IN BARBADOS.

15. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

16. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

17. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

18. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

19. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

20. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

21. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

22. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

23. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

24. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

25. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

26. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

27. Physiotherapy and occupational therapy and mild to moderate Parkinson Disease — Reply

28. Physiotherapy and occupational therapy vs no therapy in mild to moderate Parkinson disease: a randomized clinical trial

29. Clinical effectiveness and cost-effectiveness of physiotherapy and occupational therapy versus no therapy in mild to moderate Parkinson’s disease: a large pragmatic randomised controlled trial (PD REHAB)

Catalog

Searchworks

Select search scope, currently: Articles Catalog books, media & more in Jio Institute collections Articles journal articles & other e-resources

Search

Search Constraints

Refine your results

Search Limiters

Publication Year Range

Publication Type

Journal

Database

Publisher

29 results on '"Clarke, Carl"'

Search Results

Catalog

Select search scope, currently: Articles

Catalog

books, media & more in Jio Institute collections

Articles

journal articles & other e-resources