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Parkinson Disease: HELP
Articles by Adriano Chio
Based on 11 articles published since 2010
(Why 11 articles?)
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Between 2010 and 2020, A. Chiò wrote the following 11 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Editorial Divining progression in Parkinson disease with a blood test: NfL. 2019

Boylan, Laura S / Chiò, Adriano. ·From Bellevue Hospital (L.S.B.) · New York University School of Medicine (L.S.B.) · Albany-Stratton VA Medical Center, NY (L.S.B.) · Essentia Health, Duluth, MN (L.S.B.) · and "Rita Levi Montalcini" Department of Neuroscience (A.C.), University of Turin, Italy. ·Neurology · Pubmed #31420460.

ABSTRACT: -- No abstract --

2 Editorial A new scale for prognostication in Parkinson disease: Of animals and men. 2016

Chiò, Adriano / Defazio, Giovanni. ·From the "Rita Levi Montalcini" Department of Neuroscience (A.C.), University of Torino · Azienda Università Ospedale Città della Salute e della Scienza (A.C.), Torino · and Department of Basic Medical Sciences, Neuroscience and Sense Organs (G.D.), "Aldo Moro" University of Bari, Italy. ·Neurology · Pubmed #26888990.

ABSTRACT: -- No abstract --

3 Article Network Analysis Identifies Disease-Specific Pathways for Parkinson's Disease. 2018

Monti, Chiara / Colugnat, Ilaria / Lopiano, Leonardo / Chiò, Adriano / Alberio, Tiziana. ·Laboratory of Biochemistry and Functional Proteomics, Department of Science and High Technology, University of Insubria, via Manara,7, I-21052, Busto Arsizio, VA, Italy. · Center of Neuroscience, University of Insubria, Busto Arsizio, Italy. · 'Rita Levi Montalcini' Department of Neuroscience, University of Turin, Turin, Italy. · Laboratory of Biochemistry and Functional Proteomics, Department of Science and High Technology, University of Insubria, via Manara,7, I-21052, Busto Arsizio, VA, Italy. tiziana.alberio@uninsubria.it. · Center of Neuroscience, University of Insubria, Busto Arsizio, Italy. tiziana.alberio@uninsubria.it. ·Mol Neurobiol · Pubmed #28004338.

ABSTRACT: Neurodegenerative diseases are characterized by the progressive loss of specific neurons in selected regions of the central nervous system. The main clinical manifestation (movement disorders, cognitive impairment, and/or psychiatric disturbances) depends on the neuron population being primarily affected. Parkinson's disease is a common movement disorder, whose etiology remains mostly unknown. Progressive loss of dopaminergic neurons in the substantia nigra causes an impairment of the motor control. Some of the pathogenetic mechanisms causing the progressive deterioration of these neurons are not specific for Parkinson's disease but are shared by other neurodegenerative diseases, like Alzheimer's disease and amyotrophic lateral sclerosis. Here, we performed a meta-analysis of the literature of all the quantitative proteomic investigations of neuronal alterations in different models of Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis to distinguish between general and Parkinson's disease-specific pattern of neurodegeneration. Then, we merged proteomics data with genetics information from the DisGeNET database. The comparison of gene and protein information allowed us to identify 25 proteins involved uniquely in Parkinson's disease and we verified the alteration of one of them, i.e., transaldolase 1 (TALDO1), in the substantia nigra of 5 patients. By using open-source bioinformatics tools, we identified the biological processes specifically affected in Parkinson's disease, i.e., proteolysis, mitochondrion organization, and mitophagy. Eventually, we highlighted four cellular component complexes mostly involved in the pathogenesis: the proteasome complex, the protein phosphatase 2A, the chaperonins CCT complex, and the complex III of the respiratory chain.

4 Article A20 in Multiple Sclerosis and Parkinson's Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways? 2017

Perga, Simona / Martire, Serena / Montarolo, Francesca / Navone, Nicole D / Calvo, Andrea / Fuda, Giuseppe / Marchet, Alberto / Leotta, Daniela / Chiò, Adriano / Bertolotto, Antonio. ·Neurobiology Unit, Neurologia 2 - CReSM (Regional Referring Center Multiple Sclerosis), San Luigi Gonzaga University Hospital & Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano (TO), Italy. simonaperga77@gmail.com. · Neurobiology Unit, Neurologia 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin & AOU San Luigi, Regione Gonzole, 10, 10043, Orbassano, TO, Italy. simonaperga77@gmail.com. · Neurobiology Unit, Neurologia 2 - CReSM (Regional Referring Center Multiple Sclerosis), San Luigi Gonzaga University Hospital & Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano (TO), Italy. · "Rita Levi Montalcini" Department of Neuroscience, ALS (Amyotrophic Lateral Sclerosis) Expert Center (CRESLA), University of Turin & Città della Scienza e della Salute University Hospital, Turin, TO, Italy. · Division of Neurology, Martini Hospital, Turin, TO, Italy. ·Neurotox Res · Pubmed #28337659.

ABSTRACT: Chronic inflammation significantly contributes to the pathogenesis of several neurodegenerative disorders. In physiological conditions, a chronic inflammatory state is prevented through the termination of the acute inflammatory response once the triggering insult is eliminated. Several mechanisms regulate the resolution of inflammation. Among these, a potent inhibitor of the pro-inflammatory NF-kB signaling known as A20 has emerged as a key player. Recent studies have shown reduced blood levels of A20 in the patients of diverse chronic inflammatory diseases. Similar results have also been demonstrated in patients of multiple sclerosis (MS), a neurodegenerative disease characterized by persisting inflammation. In the present study, we investigate whether other similar neurodegenerative disorders such as Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS) also demonstrate deregulated levels of A20 expression as compared to healthy controls (HC) and treatment-naive MS patients. Our results confirm previous data that the A20 expression is reduced in whole blood of MS patients as compared to HC. Additionally, we demonstrate that significantly diminished A20 expression is also evident in PD patients. The dysregulation of the A20 pathway could then contribute to the persistence of inflammation in these disorders. It would thus be interesting to investigate further whether such commonly deregulated pathways between different inflammatory diseases could represent novel targets for therapy.

5 Article Specialist palliative care improves the quality of life in advanced neurodegenerative disorders: NE-PAL, a pilot randomised controlled study. 2017

Veronese, Simone / Gallo, G / Valle, A / Cugno, C / Chiò, A / Calvo, A / Cavalla, P / Zibetti, M / Rivoiro, C / Oliver, D J. ·Fondazione Assistenza e Ricerca in Oncologia (FARO) Onlus, Turin, Italy. · Department of Neuroscience, ALS Centre, University of Turin, Turin, Italy. · Agenzia Regionale Servizi Sanitari Piemonte ARESS Piemonte, Turin, Italy. · Centre for Professional Practice, University of Kent, Chatham, UK. ·BMJ Support Palliat Care · Pubmed #26182947.

ABSTRACT: BACKGROUND: This study analysed the impact on palliative care outcomes of a new specialist palliative care service for patients severely affected by amyotrophic lateral sclerosis (ALS/MND), multiple sclerosis, Parkinson's disease and related disorders (multiple system atrophy progressive supranuclear palsy, MSA-PSP). METHODS: The design followed the Medical Research Council Framework for the evaluation of complex interventions. A phase II randomised controlled trial (RCT) was undertaken comparing an immediate referral to the service (FT, fast track) to a 16-week wait (standard track (ST), standard best practice) using a parallel arm design. The main outcome measures were Quality of Life (measured with Schedule for the Evaluation of Individual Quality of Life Direct Weight, SEIQoL-DW) and burden of the carers (Caregivers Burden Inventory, CBI), with secondary outcomes of symptoms, psychosocial and spiritual issues. RESULTS: 50 patients severely affected by neurodegenerative conditions and their informal family carers were randomised: 25 FT, 25 ST. At baseline (T0), there were no differences between groups. 4 patients died during the follow-up (2 FT, 2 ST) and 2 FT patients dropped out before the end of the study. After 16 weeks (T1), FT participants scored significant improvement in the SEIQoL-DW index, pain dyspnoea sleep disturbance and bowel symptoms. CONCLUSIONS: This exploratory RCT provides evidence that no harm was experienced by SPCS for patients severely affected by neurodegenerative disorders. There was an improvement in quality of life and physical symptoms for neurological patients in palliative care. Caregiver burden was not affected by the service.

6 Article C9ORF72 intermediate repeat expansion in patients affected by atypical parkinsonian syndromes or Parkinson's disease complicated by psychosis or dementia in a Sardinian population. 2015

Cannas, Antonino / Solla, Paolo / Borghero, Giuseppe / Floris, Gian Luca / Chio, Adriano / Mascia, Marcello Mario / Modugno, Nicola / Muroni, Antonella / Orofino, Gianni / Di Stefano, Francesca / Calvo, Andrea / Moglia, Cristina / Restagno, Gabriella / Meloni, Mario / Farris, Rita / Ciaccio, Daniela / Puddu, Roberta / Vacca, Melisa Iris / Melis, Rosanna / Murru, Maria Rita / Tranquilli, Stefania / Corongiu, Daniela / Rolesu, Marcella / Cuccu, Stefania / Marrosu, Maria Giovanna / Marrosu, Francesco. ·Department of Neurology, Movement Disorders Center, Policlinico Universitario Monserrato, University of Cagliari, SS 554 Bivio per Sestu, 09042, Monserrato, Cagliari, Italy. antonino.cannas@tiscali.it. · Department of Neurology, Movement Disorders Center, Policlinico Universitario Monserrato, University of Cagliari, SS 554 Bivio per Sestu, 09042, Monserrato, Cagliari, Italy. · Dipartimento di Neuroscienze 'Rita Levi Montalcini', Centro Regionale Esperto per la SLA (CRESLA), Università di Torino, Turin, Italy. · I.R.C.C.S. Neuromed, Pozzilli, Isernia, Italy. · Laboratorio Centro Sclerosi Multipla, Ospedale Binaghi, Università di Cagliari, Monserrato, Cagliari, Italy. ·J Neurol · Pubmed #26275564.

ABSTRACT: The hexanucleotide repeat expansion GGGGCC in the C9ORF72 gene larger than 30 repeats has been identified as a major genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Recent papers investigated the possible pathogenic role and associated clinical phenotypes of intermediate C9ORF72 repeat expansion ranging between 20 and 30 repeats. Some studies suggested its pathogenicity for typical Parkinson's disease (PD), atypical parkinsonian syndromes, FTD with/without parkinsonism, and ALS with/without parkinsonism or with/without dementia. In our study, we aimed to screen patients affected by atypical parkinsonian syndromes or PD complicated by psychosis or dementia for the presence of C9ORF72 repeat expansions, and in unrelated age- and sex-matched healthy controls. Consecutive unrelated patients with atypical parkinsonian syndromes and patients with PD complicated by psychosis or dementia were included in this study. Atypical parkinsonian syndromes were further divided into two groups: one with patients who met the criteria for the classic forms of atypical parkinsonism [multiple system atrophy (MSA), Lewy body disease (LBD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD)] ;and patients who did not meet the above criteria, named non-classical atypical parkinsonism with or without dementia. Ninety-two unrelated patients (48 men, 44 women) were enrolled. None of the patients was found to be carriers of C9ORF72 repeat expansions with more than 30 repeats. Intermediate 20-30 repeat expansions were detected in four female patients (4.3 %). Three of them presented clinical features of atypical parkinsonian syndromes, two with non-classical atypical parkinsonism and dementia FTD-like, and one with non-classical atypical parkinsonism without dementia. The other patient presented clinical features of typical PD complicated by psychosis. Among 121 control subjects, none presented long or short expansion for the C9ORF72 gene. Our findings seem to support the hypothesis that the hexanucleotide expansions of C9ORF72 gene with intermediate repetitions between 20 and 29 repetitions could be associated with typical PD with psychosis or dementia and atypical parkinsonisms with dementia (non-classical atypical parkinsonism with dementia FTD-like) or without dementia (non-classical atypical parkinsonism upper MND-like), although the causal relationship is still unclear. In these latter patients, parkinsonism, more or less levodopa responsive, constituted the symptomatological central core at onset.

7 Article The role of TREM2 R47H as a risk factor for Alzheimer's disease, frontotemporal lobar degeneration, amyotrophic lateral sclerosis, and Parkinson's disease. 2015

Lill, Christina M / Rengmark, Aina / Pihlstrøm, Lasse / Fogh, Isabella / Shatunov, Aleksey / Sleiman, Patrick M / Wang, Li-San / Liu, Tian / Lassen, Christina F / Meissner, Esther / Alexopoulos, Panos / Calvo, Andrea / Chio, Adriano / Dizdar, Nil / Faltraco, Frank / Forsgren, Lars / Kirchheiner, Julia / Kurz, Alexander / Larsen, Jan P / Liebsch, Maria / Linder, Jan / Morrison, Karen E / Nissbrandt, Hans / Otto, Markus / Pahnke, Jens / Partch, Amanda / Restagno, Gabriella / Rujescu, Dan / Schnack, Cathrin / Shaw, Christopher E / Shaw, Pamela J / Tumani, Hayrettin / Tysnes, Ole-Bjørn / Valladares, Otto / Silani, Vincenzo / van den Berg, Leonard H / van Rheenen, Wouter / Veldink, Jan H / Lindenberger, Ulman / Steinhagen-Thiessen, Elisabeth / Anonymous8670828 / Teipel, Stefan / Perneczky, Robert / Hakonarson, Hakon / Hampel, Harald / von Arnim, Christine A F / Olsen, Jørgen H / Van Deerlin, Vivianna M / Al-Chalabi, Ammar / Toft, Mathias / Ritz, Beate / Bertram, Lars. ·Platform for Genome Analytics, Institutes of Neurogenetics & Integrative and Experimental Genomics, University of Lübeck, Lübeck, Germany; Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Berlin, Germany. Electronic address: christina.lill@gmx.de. · Department of Neurology, Oslo University Hospital, Oslo, Norway. · Department of Clinical Neuroscience, Institute of Psychiatry, King's College London, London, UK. · Center for Applied Genomics, Abramson Research Center, The Children's Hospital of Philadelphia, Philadelphia, PA, USA; Division of Human Genetics, Abramson Research Center, The Children's Hospital of Philadelphia, Philadelphia, PA, USA; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. · Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA. · Max Planck Institute for Human Development, Berlin, Germany. · Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark. · Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Berlin, Germany. · Department of Psychiatry and Psychotherapy, Technische Universität München, Munich, Germany. · Rita Levi Montalcini Department of Neuroscience, ALS Center, University of Torino, Torino, Italy. · Rita Levi Montalcini Department of Neuroscience, ALS Center, University of Torino, Torino, Italy; Neuroscience Institute of Turin, Turin, Italy. · Department of Neurology, Linköping University, Linköping, Sweden. · Department of Psychiatry, Psychosomatic Medicine and Psychotherapy, Goethe University of Frankfurt, Frankfurt, Germany. · Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden. · Department of Neurology, University of Ulm, Ulm, Germany. · The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. · School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK; Neurosciences Division, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK. · Department of Pharmacology, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. · Department of Neuro-/Pathology, University of Oslo and Oslo University Hospital, Oslo, Norway; Lübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany. · Department of Clinical Pathology, Molecular Genetics Unit, Azienda Ospedaliera Città della Salute e della Scienza, Torino, Italy. · Department of Psychiatry, University of Halle-Wittenberg, Halle, Germany. · Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK. · Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway. · Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milano, Italy; Department of Pathophysiology and Tranplantation, "Dino Ferrari" Center, Università degli Studi di Milano, Milano, Italy. · Department of Neurology, Neuromuscular Diseases Brain Center Rudolf Magnus, Netherlands ALS Center, University Medical Center Utrecht, Utrecht, The Netherlands. · Interdisciplinary Metabolic Center, Lipids Clinic, Charité University Medicine, Berlin, Germany. · German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany; Department of Psychosomatic Medicine, University of Rostock, Rostock, Germany. · Department of Psychiatry and Psychotherapy, Technische Universität München, Munich, Germany; Neuroepidemiology and Ageing Research Unit, School of Public Health, Faculty of Medicine, The Imperial College of Science, Technology, and Medicine, London, UK; West London Cognitive Disorders Treatment and Research Unit, West London Mental Health Trust, London, UK. · AXA Research Fund & UPMC Chair, Paris, France; Département de Neurologie, Sorbonne Universités, Université Pierre et Marie Curie, Institut de la Mémoire et de la Maladie d'Alzheimer & Institut du Cerveau et de la Moelle épinière (ICM), Hôpital de la Pitié-Salpétrière, Paris, France. · Department of Epidemiology and Environmental Sciences, School of Public Health, University of California, Los Angeles, CA, USA. · Platform for Genome Analytics, Institutes of Neurogenetics & Integrative and Experimental Genomics, University of Lübeck, Lübeck, Germany; Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Berlin, Germany; Neuroepidemiology and Ageing Research Unit, School of Public Health, Faculty of Medicine, The Imperial College of Science, Technology, and Medicine, London, UK. ·Alzheimers Dement · Pubmed #25936935.

ABSTRACT: A rare variant in TREM2 (p.R47H, rs75932628) was recently reported to increase the risk of Alzheimer's disease (AD) and, subsequently, other neurodegenerative diseases, i.e. frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). Here we comprehensively assessed TREM2 rs75932628 for association with these diseases in a total of 19,940 previously untyped subjects of European descent. These data were combined with those from 28 published data sets by meta-analysis. Furthermore, we tested whether rs75932628 shows association with amyloid beta (Aβ42) and total-tau protein levels in the cerebrospinal fluid (CSF) of 828 individuals with AD or mild cognitive impairment. Our data show that rs75932628 is highly significantly associated with the risk of AD across 24,086 AD cases and 148,993 controls of European descent (odds ratio or OR = 2.71, P = 4.67 × 10(-25)). No consistent evidence for association was found between this marker and the risk of FTLD (OR = 2.24, P = .0113 across 2673 cases/9283 controls), PD (OR = 1.36, P = .0767 across 8311 cases/79,938 controls) and ALS (OR = 1.41, P = .198 across 5544 cases/7072 controls). Furthermore, carriers of the rs75932628 risk allele showed significantly increased levels of CSF-total-tau (P = .0110) but not Aβ42 suggesting that TREM2's role in AD may involve tau dysfunction.

8 Article The p.A382T TARDBP gene mutation in Sardinian patients affected by Parkinson's disease and other degenerative parkinsonisms. 2013

Cannas, Antonino / Borghero, Giuseppe / Floris, Gian Luca / Solla, Paolo / Chiò, Adriano / Traynor, Bryan J / Calvo, Andrea / Restagno, Gabriella / Majounie, Elisa / Costantino, Emanuela / Piras, Valeria / Lavra, Loredana / Pani, Carla / Orofino, Gianni / Di Stefano, Francesca / Tacconi, Paolo / Mascia, Marcello Mario / Muroni, Antonella / Murru, Maria Rita / Tranquilli, Stefania / Corongiu, Daniela / Rolesu, Marcella / Cuccu, Stefania / Marrosu, Francesco / Marrosu, Maria Giovanna. ·Centro per i Disordini del Movimento, Dipartimento di Scienze Cardiovascolari e Neurologiche, Sezione Neurologia, Policlinico Universitario, Università di Cagliari, SS 554 Bivio Sestu, 09042 Monserrato, Cagliari, Italy. antonino.cannas@tiscali.it ·Neurogenetics · Pubmed #23546887.

ABSTRACT: Based on our previous finding of the p.A382T founder mutation in ALS patients with concomitant parkinsonism in the Sardinian population, we hypothesized that the same variant may underlie Parkinson's disease (PD) and/or other forms of degenerative parkinsonism on this Mediterranean island. We screened a cohort of 611 patients with PD (544 cases) and other forms of degenerative parkinsonism (67 cases) and 604 unrelated controls for the c.1144G > A (p.A382T) missense mutation of the TARDBP gene. The p.A382T mutation was identified in nine patients with parkinsonism. Of these, five (0.9 % of PD patients) presented a typical PD (two with familiar forms), while four patients (6.0 % of all other forms of parkinsonism) presented a peculiar clinical presentation quite different from classical atypical parkinsonism with an overlap of extrapyramidal-pyramidal-cognitive clinical signs. The mutation was found in eight Sardinian controls (1.3 %) consistent with a founder mutation in the island population. Our findings suggest that the clinical presentation of the p.A382T TARDBP gene mutation may include forms of parkinsonism in which the extrapyramidal signs are the crucial core of the disease at onset. These forms can present PSP or CBD-like clinical signs, with bulbar and/or extrabulbar pyramidal signs and cognitive impairment. No evidence of association has been found between TARDBP gene mutation and typical PD.

9 Article Mutational analysis of the VCP gene in Parkinson's disease. 2012

Majounie, Elisa / Traynor, Bryan J / Chiò, Adriano / Restagno, Gabriella / Mandrioli, Jessica / Benatar, Michael / Taylor, J Paul / Singleton, Andrew B. ·Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD, USA. Elisa.Majounie@nih.gov ·Neurobiol Aging · Pubmed #21920633.

ABSTRACT: Mutations in the valosin-containing protein gene (VCP) have been identified in neurological disorders (inclusion body myopathy--early Paget's disease of the bone--frontotemporal dementia and amyotrophic lateral sclerosis) and are thought to play a role in the clearance of abnormally folded proteins. Parkinsonism has been noted in kindreds with VCP mutations. Based on this, we hypothesized that mutations in VCP may also contribute to idiopathic Parkinson's disease (PD). We screened the coding region of the VCP gene in a large cohort of 768 late-onset PD cases (average age at onset, 70 years), both sporadic and with positive family history. We identified a number of rare single nucleotide changes, including a variant previously described to be pathogenic, but no clear disease-causing variants. We conclude that mutations in VCP are not a common cause for idiopathic PD.

10 Minor NADPH oxidases 2 activation in patients with Parkinson's disease. 2018

Marrali, G / Casale, F / Salamone, P / Fuda, G / Ilardi, A / Manera, U / Calvo, A / Zibetti, M / Lopiano, L / Chiò, A. ·Department of Neuroscience 'Rita Levi Montalcini', University of Torino, Italy. · Department of Neuroscience 'Rita Levi Montalcini', University of Torino, Italy. Electronic address: federico.casale@unito.it. ·Parkinsonism Relat Disord · Pubmed #29331562.

ABSTRACT: -- No abstract --

11 Minor C9ORF72 and parkinsonism: Weak link, innocent bystander, or central player in neurodegeneration? 2017

Cavallieri, Francesco / Mandrioli, Jessica / Rosafio, Francesca / Contardi, Sara / Fasano, Antonio / Menozzi, Elisa / Caponnetto, Claudia / Chiò, Adriano / Valzania, Franco. ·Department of Neuroscience, St. Agostino Estense Hospital, University of Modena and Reggio Emilia, Modena, Italy. Electronic address: cava_87@hotmail.it. · Department of Neuroscience, St. Agostino Estense Hospital, University of Modena and Reggio Emilia, Modena, Italy. Electronic address: j.mandrioli@ausl.mo.it. · Department of Neuroscience, St. Agostino Estense Hospital, University of Modena and Reggio Emilia, Modena, Italy. · U.O. Neurology, IRCCS AOU S. Martino-IST, Largo R. Benzi, Genoa, Italy. Electronic address: ccaponnetto@neurologia.unige.it. · Azienda Ospedaliero-Universitaria Città della Salute e della Scienza, Torino, Italy; ALS Center, 'Rita Levi Montalcini' Department of Neuroscience, Neurology II, University of Torino, Turin, Italy. Electronic address: adriano.chio@unito.it. ·J Neurol Sci · Pubmed #28566177.

ABSTRACT: -- No abstract --