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1. Depressive symptoms in Parkinson's disease are related to reduced [123I]FP-CIT binding in the caudate nucleus

Author

Chris Vriend, Elisabeth M. J. Foncke, Jan Smit, Karin D. van Dijk, Ysbrand D. van der Werf, Henk W. Berendse, Odile A. van den Heuvel, Pieter G. Raijmakers, Dick J. Veltman, Netherlands Institute for Neuroscience (NIN), Neuroscience Campus Amsterdam - Neurodegeneration, Psychiatry, Anatomy and neurosciences, Radiology and nuclear medicine, Neurology, and NCA - neurodegeneration

Subjects
Male, Parkinson's disease, Caudate nucleus, Striatum, Iodine Radioisotopes, SDG 3 - Good Health and Well-being, Dopamine, medicine, Humans, Radionuclide Imaging, Aged, Retrospective Studies, Dopamine transporter, Dopamine Plasma Membrane Transport Proteins, biology, Depression, Putamen, Dopaminergic, Parkinson Disease, Middle Aged, medicine.disease, Ventral tegmental area, Psychiatry and Mental health, Cross-Sectional Studies, medicine.anatomical_structure, nervous system, biology.protein, Female, Surgery, Neurology (clinical), Caudate Nucleus, Psychology, Neuroscience, Tropanes, medicine.drug
Abstract

Background Depression is a common neuropsychiatric symptom in Parkinson9s disease (PD). In previous research, PD-related depression was associated with striatal dopaminergic deficits, presumably due to degeneration of brainstem dopaminergic projections. Segregated areas of the striatum are crucially involved in various parallelly arranged cortical-striatal-thalamocortical circuits and serve functions in, among others, motor control or emotion. This suggests regional specificity of dopaminergic deficits in the striatum in motor and depressive symptoms in PD. Methods In this cross-sectional retrospective study, we correlated severity scores of depressive and motor symptoms in 100 non-demented PD patients (median Hoehn & Yahr stage: 2) with dopamine loss in specific regions of the striatum as measured by [ 123 I]FP-CIT SPECT tracer binding to the dopamine transporter (DaT). Results Depressive symptoms were related to lower DaT binding in the right caudate nucleus, while motor symptoms were associated with decreased DaT binding in the right putamen. This double dissociation was most pronounced in early-stage PD patients. Conclusions These results suggest that depressive symptoms in PD are associated with dopamine loss in the caudate nucleus, possibly related to degeneration of dopaminergic projections from the ventral tegmental area, while motor symptoms are associated with low dopamine signalling to the putamen and loss of nigrostriatal projections. This is consistent with the neuroanatomy of partially segregated cortical-striatal-thalamocortical circuits and supports the role of dysfunctional associative and motivational circuits in PD-related depression.

Published
2013

2. Loss of VPS13C Function in Autosomal-Recessive Parkinsonism Causes Mitochondrial Dysfunction and Increases PINK1/Parkin-Dependent Mitophagy

Author

Suzanne Lesage, Valérie Drouet, Elisa Majounie, Vincent Deramecourt, Maxime Jacoupy, Aude Nicolas, Florence Cormier-Dequaire, Sidi Mohamed Hassoun, Claire Pujol, Sorana Ciura, Zoi Erpapazoglou, Tatiana Usenko, Claude-Alain Maurage, Mourad Sahbatou, Stefan Liebau, Jinhui Ding, Basar Bilgic, Murat Emre, Nihan Erginel-Unaltuna, Gamze Guven, François Tison, Christine Tranchant, Marie Vidailhet, Jean-Christophe Corvol, Paul Krack, Anne-Louise Leutenegger, Michael A. Nalls, Dena G. Hernandez, Peter Heutink, J. Raphael Gibbs, John Hardy, Nicholas W. Wood, Thomas Gasser, Alexandra Durr, Jean-François Deleuze, Meriem Tazir, Alain Destée, Ebba Lohmann, Edor Kabashi, Andrew Singleton, Olga Corti, Alexis Brice, Yves Agid, Mathieu Anheim, Anne-Marie Bonnet, Michel Borg, Emmanuel Broussolle, Philippe Damier, Alexandra Dürr, Franck Durif, Stephan Klebe, Maria Martinez, Pierre Pollak, Olivier Rascol, Marc Vérin, François Viallet, Jean Christophe Corvol, Sampath Arepalli, Roger A. Barker, Yoav Ben-Shlomo, Daniela Berg, Francesco Bettella, Kailash Bhatia, Rob M.A. de Bie, Alessandro Biffi, Bastiaan R. Bloem, Zoltan Bochdanovits, Michael Bonin, Jose M. Bras, Kathrin Brockmann, Janet Brooks, David J. Burn, Gavin Charlesworth, Honglei Chen, Patrick F. Chinnery, Sean Chong, Carl E. Clarke, Mark R. Cookson, Carl Counsell, Jean-François Dartigues, Panos Deloukas, Günther Deuschl, David T. Dexter, Karin D. van Dijk, Allissa Dillman, Jing Dong, Frank Durif, Sarah Edkins, Valentina Escott-Price, Jonathan R. Evans, Thomas Foltynie, Jianjun Gao, Michelle Gardner, Alison Goate, Emma Gray, Rita Guerreiro, Clare Harris, Jacobus J. van Hilten, Albert Hofman, Albert Hollenbeck, Peter Holmans, Janice Holton, Michèle Hu, Xuemei Huang, Heiko Huber, Gavin Hudson, Sarah E. Hunt, Johanna Huttenlocher, Thomas Illig, Pálmi V. Jónsson, Laura L. Kilarski, Iris E. Jansen, Jean-Charles Lambert, Cordelia Langford, Andrew Lees, Peter Lichtner, Patricia Limousin, Grisel Lopez, Delia Lorenz, Steven Lubbe, Codrin Lungu, María Martinez, Walter Mätzler, Alisdair McNeill, Catriona Moorby, Matthew Moore, Karen E. Morrison, Ese Mudanohwo, Sean S. O’Sullivan, Michael J. Owen, Justin Pearson, Joel S. Perlmutter, Hjörvar Pétursson, Vincent Plagnol, Bart Post, Simon Potter, Bernard Ravina, Tamas Revesz, Olaf Riess, Fernando Rivadeneira, Patrizia Rizzu, Mina Ryten, Mohamad Saad, Javier Simón-Sánchez, Stephen Sawcer, Anthony Schapira, Hans Scheffer, Claudia Schulte, Manu Sharma, Karen Shaw, Una-Marie Sheerin, Ira Shoulson, Joshua Shulman, Ellen Sidransky, Chris C.A. Spencer, Hreinn Stefánsson, Kári Stefánsson, Joanna D. Stockton, Amy Strange, Kevin Talbot, Carlie M. Tanner, Avazeh Tashakkori-Ghanbaria, Daniah Trabzuni, Bryan J. Traynor, André G. Uitterlinden, Daan Velseboer, Robert Walker, Bart van de Warrenburg, Mirdhu Wickremaratchi, Caroline H. Williams-Gray, Sophie Winder-Rhodes, Isabel Wurster, Nigel Williams, Huw R. Morris, Andrew B. Singleton, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, Complex Trait Genetics, Neurology, Graduate School, ANS - Cellular & Molecular Mechanisms, Krack, Paul, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Department of Neurodegenerative Diseases, Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, Laboratory of Neurogenetics, National Institute of Aging, Département d'histologie et de pathologie, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre d'investigation clinique Neurosciences [CHU Pitié Salpêtrière] (CIC Neurosciences), CHU Pitié-Salpêtrière [AP-HP], Fondation Jean Dausset CEPH, Institute of Neuroanatomy, Department of Neurology, Behavioural Neurology and Movement Disorders Unit, Istanbul Faculty of Medicine, Istanbul University, Department of Genetics, Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Pôle Tête-Cou-CETD, Les Hôpitaux Universitaires de Strasbourg (HUS), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Département de neurologie, Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble, Variabilité Génétique et Maladies Humaines, Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot - Paris 7 (UPD7), Hertie Institute for Clinical Brain Research [Tubingen], University of Tübingen, Department of Molecular Neuroscience, University College of London [London] (UCL)-Institute of Neurology, Service de génétique, cytogénétique, embryologie [Pitié-Salpétrière], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Pierre et Marie Curie - Paris 6 (UPMC), Commissariat à l'Energie Atomique Saclay, Service de Neurologie, CHU Mustapha, Movement Disorders Unit, HAL-UPMC, Gestionnaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Centre d'investigation clinique pluridisciplinaire [CHU Pitié Salpêtrière] (CIC-P 1421), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de génétique, cytogénétique, embryologie [CHU Pitié-Salpétrière], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)

Subjects
0301 basic medicine, Male, Turkey, parkin protein, Mitochondrion, Compound heterozygosity, Parkin, Proteins/*genetics/metabolism, Consanguinity, 0302 clinical medicine, diagnosis [Parkinsonian Disorders], Mitophagy, Genetics(clinical), metabolism [Protein Kinases], Cognitive decline, Genetics (clinical), Exome sequencing, genetics [Ubiquitin-Protein Ligases], Genetics, Parkinsonism, genetics [Protein Kinases], Homozygote, metabolism [Proteins], Middle Aged, Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3], Pedigree, Phenotype, genetics [Parkinsonian Disorders], COS Cells, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Female, Parkinsonian Disorders/diagnosis/*genetics, Protein Kinases/*genetics/metabolism, PTEN-induced putative kinase, Adult, Heterozygote, Mitochondrial Degradation/*genetics, Ubiquitin-Protein Ligases, PINK1, Biology, VPS13C protein, human, 03 medical and health sciences, Genetic Heterogeneity, metabolism [Ubiquitin-Protein Ligases], Parkinsonian Disorders, ddc:570, medicine, Animals, Humans, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Gene Silencing, Aged, Proteins, Reproducibility of Results, medicine.disease, genetics [Proteins], ddc:616.8, Ubiquitin-Protein Ligases/*genetics/metabolism, 030104 developmental biology, HEK293 Cells, Case-Control Studies, Protein Kinases, 030217 neurology & neurosurgery, genetics [Mitophagy]
Abstract

Contains fulltext : 167923.pdf (Publisher’s version ) (Open Access) Autosomal-recessive early-onset parkinsonism is clinically and genetically heterogeneous. The genetic causes of approximately 50% of autosomal-recessive early-onset forms of Parkinson disease (PD) remain to be elucidated. Homozygozity mapping and exome sequencing in 62 isolated individuals with early-onset parkinsonism and confirmed consanguinity followed by data mining in the exomes of 1,348 PD-affected individuals identified, in three isolated subjects, homozygous or compound heterozygous truncating mutations in vacuolar protein sorting 13C (VPS13C). VPS13C mutations are associated with a distinct form of early-onset parkinsonism characterized by rapid and severe disease progression and early cognitive decline; the pathological features were striking and reminiscent of diffuse Lewy body disease. In cell models, VPS13C partly localized to the outer membrane of mitochondria. Silencing of VPS13C was associated with lower mitochondrial membrane potential, mitochondrial fragmentation, increased respiration rates, exacerbated PINK1/Parkin-dependent mitophagy, and transcriptional upregulation of PARK2 in response to mitochondrial damage. This work suggests that loss of function of VPS13C is a cause of autosomal-recessive early-onset parkinsonism with a distinctive phenotype of rapid and severe progression.

Published
2016

3. The proteome of the locus ceruleus in Parkinson's disease: relevance to pathogenesis

Author

Karin D, van Dijk, Henk W, Berendse, Benjamin, Drukarch, Silvina A, Fratantoni, Thang V, Pham, Sander R, Piersma, Evelien, Huisman, John J P, Brevé, Henk J, Groenewegen, Connie R, Jimenez, and Wilma D J, van de Berg

Subjects
Aged, 80 and over, Male, Proteome, Tandem Mass Spectrometry, Blotting, Western, Humans, Female, Locus Coeruleus, Parkinson Disease, Comet Assay, Immunohistochemistry, Research Articles, Aged
Abstract

The locus ceruleus is among the earliest affected brain regions in Parkinson's disease (PD) showing Lewy body pathology and neuronal loss. To improve our understanding of the pathogenesis of PD, we performed the first proteomic analysis ever of post‐mortem locus ceruleus tissue of six pathologically confirmed PD patients, and six age‐ and gender‐matched non‐neurological controls. In total 2495 proteins were identified, of which 87 proteins were differentially expressed in the locus ceruleus of PD patients compared with controls. The majority of these differentially expressed proteins are known to be involved in processes that have been implicated in the pathogenesis of PD previously, including mitochondrial dysfunction, oxidative stress, protein misfolding, cytoskeleton dysregulation and inflammation. Several individual proteins were identified that have hitherto not been associated with PD, such as regucalcin, which plays a role in maintaining intracellular calcium homeostasis, and isoform 1 of kinectin, which is involved in transport of cellular components along microtubules. In addition, pathway analysis suggests a pathogenetic role for aminoacyl‐tRNA‐biosynthesis. These findings indicate that the proteome of the locus ceruleus of PD patients and non‐neurological controls provides data that are relevant to the pathogenesis of PD, reflecting both known and potentially novel pathogenetic pathways.

Published
2011

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