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Parkinson Disease: HELP
Articles from Milan area
Based on 532 articles published since 2008
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These are the 532 published articles about Parkinson Disease that originated from Milan area during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
1 Editorial The need for an extensive neuropsychological assessment for a reliable diagnosis of mild cognitive impairment in patients with Parkinson's disease. 2018

Daniele, A / Lacidogna, G. ·Institute of Neurology, Catholic University of Sacred Heart, Rome, Italy. ·Eur J Neurol · Pubmed #29509993.

ABSTRACT: -- No abstract --

2 Editorial Can a cognitive rehabilitation program in early stages of Parkinson's disease improve cognition, apathy and brain functional connectivity for up to 18 months? 2018

Daniele, A / Panza, F. ·Institute of Neurology, Catholic University of Sacred Heart, Rome, Italy. · Geriatric Unit and Gerontology-Geriatrics Research Laboratory, Department of Medical Sciences, IRCCS 'Casa Sollievo della Sofferenza', San Giovanni Rotondo, Italy. · Neurodegenerative Disease Unit, Department of Basic Medicine, Neuroscience and Sense Organs, University of Bari 'Aldo Moro', Bari, Italy. · Neurodegenerative Disease Unit, Department of Clinical Research in Neurology, University of Bari 'Aldo Moro', Azienda Ospedaliera 'Card. G. Panico', Tricase, Italy. ·Eur J Neurol · Pubmed #29215769.

ABSTRACT: -- No abstract --

3 Editorial Classifying tremor: Language matters. 2018

Albanese, Alberto. ·Department of Neurology, Humanitas Research Hospital, Rozzano, Milano, Italy. · Department of Neurology, Catholic University, Milano, Italy. ·Mov Disord · Pubmed #29193400.

ABSTRACT: -- No abstract --

4 Editorial GTP cyclohydrolase 1 mutations and Parkinson's disease: new insights beyond DOPA-responsive dystonia. 2015

Carecchio, Miryam / Schneider, Susanne A. ·Molecular Neurogentics Unit, C. Besta Institute, Milan, Italy. · Neurology Department, University of Kiel, Kiel, Germany. ·Mov Disord · Pubmed #26012785.

ABSTRACT: -- No abstract --

5 Editorial Novel perspectives for Parkinson's disease therapy: insights from the latest advances in disease pathophysiology, diagnostic and experimental tools and molecular targets. 2013

Spano, Pier Franco / Bellucci, Arianna. ·Department of Molecular and Translational Medicine National Institute of Neuroscience University of Brescia Brescia Italy. bellucci@med.unibs.it. ·CNS Neurol Disord Drug Targets · Pubmed #24040812.

ABSTRACT: -- No abstract --

6 Review α-Synuclein and Glia in Parkinson's Disease: A Beneficial or a Detrimental Duet for the Endo-Lysosomal System? 2019

Filippini, Alice / Gennarelli, Massimo / Russo, Isabella. ·Biology and Genetic Unit, Department of Molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. · Genetics Unit, IRCCS Istituto Centro S. Giovanni di Dio, Fatebenefratelli, 25123, Brescia, Italy. · Biology and Genetic Unit, Department of Molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. isabella.russo@unibs.it. ·Cell Mol Neurobiol · Pubmed #30637614.

ABSTRACT: Accumulation of α-synuclein (α-syn) species in dopaminergic neurons is one of the main hallmarks of Parkinson's disease (PD). Several factors have been associated with α-syn aggregation process, including an impairment of the proper protein degradation, which might drive the neurons toward an alternative and/or additional clearance mechanism that involves the release of undigested material from the cell. It has been reported that extracellular α-syn, released by stressed and/or degenerating neurons, might widely contribute to the neuronal toxicity and degeneration. Therefore, the uptake and clearance of misfolded/aggregated proteins is a key process to control extracellular deposition of α-syn aggregates, the spreading and progression of the disease. All the main brain cell types, neurons, astrocytes and microglia are able to internalize and degrade extracellular α-syn, however, glial cells appear to be the most efficient scavengers. Accumulating evidence indicates that the endocytosis of α-syn species might be conformation-sensitive, cell- and receptor-type specific, making the scenario highly complex. In this review, we will shed light on the different endocytosis mechanisms and receptors recruited for the uptake and clearance of pathological α-syn forms with a special focus on glial cells. Moreover, we will discuss how PD-related genes, in addition to α-syn itself, may alter the endo-lysosomal pathway causing an impairment of clearance, which, in turn, lead to accumulation of toxic species, dysfunctions of glia physiology and progression of the disease.

7 Review Living in Promiscuity: The Multiple Partners of Alpha-Synuclein at the Synapse in Physiology and Pathology. 2019

Longhena, Francesca / Faustini, Gaia / Spillantini, Maria Grazia / Bellucci, Arianna. ·Division of Pharmacology, Department of molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. f.longhena@unibs.it. · Division of Pharmacology, Department of molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. g.faustini004@unibs.it. · Department of Clinical Neurosciences, Clifford Allbutt Building, University of Cambridge, Cambridge CB2 0AH, UK. mgs11@cam.ac.uk. · Division of Pharmacology, Department of molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. arianna.bellucci@unibs.it. · Laboratory for Preventive and Personalized Medicine, Department of molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123, Brescia, Italy. arianna.bellucci@unibs.it. ·Int J Mol Sci · Pubmed #30609739.

ABSTRACT: Alpha-synuclein (α-syn) is a small protein that, in neurons, localizes predominantly to presynaptic terminals. Due to elevated conformational plasticity, which can be affected by environmental factors, in addition to undergoing disorder-to-order transition upon interaction with different interactants, α-syn is counted among the intrinsically disordered proteins (IDPs) family. As with many other IDPs, α-syn is considered a hub protein. This function is particularly relevant at synaptic sites, where α-syn is abundant and interacts with many partners, such as monoamine transporters, cytoskeletal components, lipid membranes, chaperones and synaptic vesicles (SV)-associated proteins. These protein⁻protein and protein⁻lipid membrane interactions are crucial for synaptic functional homeostasis, and alterations in α-syn can cause disruption of this complex network, and thus a failure of the synaptic machinery. Alterations of the synaptic environment or post-translational modification of α-syn can induce its misfolding, resulting in the formation of oligomers or fibrillary aggregates. These α-syn species are thought to play a pathological role in neurodegenerative disorders with α-syn deposits such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), which are referred to as synucleinopathies. Here, we aim at revising the complex and promiscuous role of α-syn at synaptic terminals in order to decipher whether α-syn molecular interactants may influence its conformational state, contributing to its aggregation, or whether they are just affected by it.

8 Review Pharmacokinetic drug evaluation of CVT-301 for the treatment of Parkinson's disease. 2018

Stocchi, Fabrizio / Vacca, Laura / Stirpe, Paola / Torti, Margherita. ·a Departement of Neurology , University and Institute for Research and Medical Care, San Raffaele Rome , Roma , Italy. · b Department of Neurorehabilitation Sciences , Casa Cura Policlinico (CCP) , Milan , Italy. · c Departement of Neurology , Institute for Research and Medical Care, San Raffaele Cassino , Cassino (FR) , Italy. ·Expert Opin Drug Metab Toxicol · Pubmed #30479171.

ABSTRACT: INTRODUCTION: Levodopa (LD), in combination with a decarboxylase inhibitor, is a mainstay and the most effective therapeutic agent in the treatment of Parkinson's disease (PD). Unfortunately, during chronic treatment with this agent, ON-OFF phenomena and dyskinesia appear. Despite the many medical treatment options available, unpredictable OFF episodes can still occur and be severe and disabling. A rescue therapy that provides a rapid and predictable ON response for patients with OFF periods would be of great value for such patients. Areas covered: CVT-301 is a self-administered dry powder aerosol inhaled formulation of LD that is being developed as a self-administered treatment for OFF periods. The PK profile of CVT-301, the efficacy, and the safety highlighted in randomized clinical trials will be reviewed. Expert opinion: CVT-301 may offer several potential advantages including increased systemic bioavailability through pulmonary absorption, rapid onset of action, avoidance of first-pass drug metabolism and less plasma-level variability. List of Abbreviations: PD: Parkinson's disease; LD: Levodopa; CD: Carbidopa; AADC: aromatic L-amino acid decarboxylase; IR: immediate-release; FPD: fine particle dose; GI: gastrointestinal; PK: pharmacokinetic; CVs: coefficient of variation; UPDRS: Unified Parkinson's Disease Rating Scale; AEs: adverse events; FEV: forced expiratory volume; FVC: forced vital capacity; DL

9 Review Functional MRI in Idiopathic Parkinson's Disease. 2018

Filippi, Massimo / Elisabetta, Sarasso / Piramide, Noemi / Agosta, Federica. ·Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University, Milan, Italy; Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. Electronic address: filippi.massimo@hsr.it. · Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University, Milan, Italy; Laboratory of Movement Analysis, San Raffaele Scientific Institute, Milan, Italy. · Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University, Milan, Italy. ·Int Rev Neurobiol · Pubmed #30314606.

ABSTRACT: Functional MRI (fMRI) has been widely used to study abnormal patterns of brain connectivity at rest and activation during a variety of tasks in patients with idiopathic Parkinson's disease (PD). fMRI studies in PD have led to a better understanding of many aspects of the disease including both motor and non-motor symptoms. Although its translation into clinical practice is still at an early stage, fMRI measures hold promise for multiple clinical applications in PD, including the early detection, predicting future change in clinical status, and as a marker of alterations in brain physiology related to neurotherapeutic agents and neurorehabilitative strategies.

10 Review Molecular Imaging of the Cannabinoid System in Idiopathic Parkinson's Disease. 2018

Cilia, Roberto. ·Parkinson Institute, ASST Gaetano Pini-CTO, Milan, Italy. Electronic address: roberto.cilia@gmail.com. ·Int Rev Neurobiol · Pubmed #30314601.

ABSTRACT: The endocannabinoid system is a modulator of neurotransmitter release and is involved in several physiological functions. Hence, it has been increasingly studied as a potential pharmacologic target of Parkinson's disease. Several preclinical and clinical studies evidenced a substantial rearrangement of the endocannabinoid system in the basal ganglia circuit following dopamine depletion. The endocannabinoid system has been additionally implicated in the regulation of neuroinflammation and neuroprotection through the activation of CB2 receptors, suggesting a potential target for disease modifying therapies in Parkinson's disease. In this chapter, current pharmacological and physiological knowledge on the role of the endocannabinoid system will be reviewed, focusing on preclinical studies animal models and clinical studies in patients with idiopathic Parkinson's disease. The main strategies for imaging the brain cannabinoid system will be summarized to finally focus on in vivo imaging of patients with Parkinson's disease.

11 Review Istradefylline for the treatment of Parkinson's disease: is it a promising strategy? 2018

Torti, Margherita / Vacca, Laura / Stocchi, Fabrizio. ·a Center for Parkinson's Disease , IRCCS San Raffaele Pisana , Rome , Italy. · b Neurology Department , San Raffaele Cassino , Cassino , Italy. · c Neurology Department , Casa di Cura Privata Policlinico (CCPP) , Milan , Italy. · d Neurology Department , San Raffaele University , Rome , Italy. ·Expert Opin Pharmacother · Pubmed #30232916.

ABSTRACT: INTRODUCTION: Istradefylline (ISD) is a new drug developed for the treatment of Parkinson's disease (PD). It is an adenosine receptor A

12 Review Clinical utility of FDG PET in Parkinson's disease and atypical parkinsonism associated with dementia. 2018

Walker, Zuzana / Gandolfo, Federica / Orini, Stefania / Garibotto, Valentina / Agosta, Federica / Arbizu, Javier / Bouwman, Femke / Drzezga, Alexander / Nestor, Peter / Boccardi, Marina / Altomare, Daniele / Festari, Cristina / Nobili, Flavio / Anonymous2310976. ·Division of Psychiatry, University College London, London, UK. z.walker@ucl.ac.uk. · St Margaret's Hospital, Essex Partnership University NHS Foundation Trust, Epping, CM16 6TN, UK. z.walker@ucl.ac.uk. · Alzheimer Operative Unit, IRCCS S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy. · Division of Nuclear Medicine and Molecular Imaging, Department of Medical Imaging, University Hospitals of Geneva, Geneva University, Geneva, Switzerland. · Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. · Department of Nuclear Medicine, Clinica Universidad de Navarra, University of Navarra, Pamplona, Spain. · Department of Neurology & Alzheimer Center, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands. · Department of Nuclear Medicine, University Hospital of Cologne, University of Cologne and German Center for Neurodegenerative Diseases (DZNE), Cologne, Germany. · German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. · Queensland Brain Institute, University of Queensland and the Mater Hospital, Brisbane, Australia. · LANVIE (Laboratoire de Neuroimagerie du Vieillissement), Department of Psychiatry, University of Geneva, Geneva, Switzerland. · LANE - Laboratory of Alzheimer's Neuroimaging & Epidemiology, IRCCS S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy. · Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. · Department of Neuroscience (DINOGMI), University of Genoa & Clinical Neurology Polyclinic IRCCS San Martino-IST, Genoa, Italy. flaviomariano.nobili@hsanmartino.it. ·Eur J Nucl Med Mol Imaging · Pubmed #29779045.

ABSTRACT: PURPOSE: There are no comprehensive guidelines for the use of FDG PET in the following three clinical scenarios: (1) diagnostic work-up of patients with idiopathic Parkinson's disease (PD) at risk of future cognitive decline, (2) discriminating idiopathic PD from progressive supranuclear palsy, and (3) identifying the underlying neuropathology in corticobasal syndrome. METHODS: We therefore performed three literature searches and evaluated the selected studies for quality of design, risk of bias, inconsistency, imprecision, indirectness and effect size. Critical outcomes were the sensitivity, specificity, accuracy, positive/negative predictive value, area under the receiving operating characteristic curve, and positive/negative likelihood ratio of FDG PET in detecting the target condition. Using the Delphi method, a panel of seven experts voted for or against the use of FDG PET based on published evidence and expert opinion. RESULTS: Of 91 studies selected from the three literature searches, only four included an adequate quantitative assessment of the performance of FDG PET. The majority of studies lacked robust methodology due to lack of critical outcomes, inadequate gold standard and no head-to-head comparison with an appropriate reference standard. The panel recommended the use of FDG PET for all three clinical scenarios based on nonquantitative evidence of clinical utility. CONCLUSION: Despite widespread use of FDG PET in clinical practice and extensive research, there is still very limited good quality evidence for the use of FDG PET. However, in the opinion of the majority of the panellists, FDG PET is a clinically useful imaging biomarker for idiopathic PD and atypical parkinsonism associated with dementia.

13 Review Basal ganglia and beyond: The interplay between motor and cognitive aspects in Parkinson's disease rehabilitation. 2018

Ferrazzoli, Davide / Ortelli, Paola / Madeo, Graziella / Giladi, Nir / Petzinger, Giselle M / Frazzitta, Giuseppe. ·Department of Parkinson's Disease, Movement Disorders and Brain Injury Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini, 3, Gravedona ed Uniti, 22015, Como, Italy. Electronic address: davideferrazzoli@gmail.com. · Department of Parkinson's Disease, Movement Disorders and Brain Injury Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini, 3, Gravedona ed Uniti, 22015, Como, Italy. Electronic address: paola.ortelli@ospedaledigravedona.it. · Department of Parkinson's Disease, Movement Disorders and Brain Injury Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini, 3, Gravedona ed Uniti, 22015, Como, Italy. Electronic address: graziella.madeo@ospedaledigravedona.it. · Movement Disorders Unit, Neurological Institute, Tel-Aviv Medical Centre, Sieratzki Chair in Neurology, Sackler School of Medicine, Sagol School for Neuroscience, Tel-Aviv University, Tel-Aviv, Israel. Electronic address: nirg@tlvmc.gov.il. · Department of Neurology, University of Southern California, Los Angeles, CA, 90033, United States; Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, 90033, United States. Electronic address: petzinge@med.usc.edu. · Department of Parkinson's Disease, Movement Disorders and Brain Injury Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini, 3, Gravedona ed Uniti, 22015, Como, Italy. Electronic address: giuseppe.frazzitta@ospedaledigravedona.it. ·Neurosci Biobehav Rev · Pubmed #29733882.

ABSTRACT: Parkinson's disease (PD) is characterized by motor and cognitive dysfunctions, affecting the motor behaviour. We summarize evidence that the interplay between motor and cognitive approaches is crucial in PD rehabilitation. Rehabilitation is complementary to pharmacological therapy and effective in reducing the PD disturbances, probably acting by inducing neuroplastic effects. The motor behaviour results from a complex integration between cortical and subcortical areas, underlying the motor, cognitive and motivational aspects of movement. The close interplay amongst these areas makes possible to learn, control and express habitual-automatic actions, which are dysfunctional in PD. The physiopathology of PD could be considered the base for the development of effective rehabilitation treatments. As the volitional action control is spared in early-medium stages of disease, rehabilitative approaches engaging cognition permit to achieve motor benefits and appear to be the most effective for PD. We will point out data supporting the relevance of targeting both motor and cognitive aspects in PD rehabilitation. Finally, we will discuss the role of cognitive engagement in motor rehabilitation for PD.

14 Review Surgical treatment of spinal disorders in Parkinson's disease. 2018

Galbusera, Fabio / Bassani, Tito / Stucovitz, Elena / Martini, Carlotta / Ismael Aguirre, Maryem-Fama / Berjano, Pedro L / Lamartina, C. ·Laboratory of Biological Structures Mechanics, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy. · G Spine 4, IRCCS Istituto Ortopedico Galeazzi, Via Galeazzi 4, 20161, Milan, Italy. martini.carlotta@gmail.com. · G Spine 4, IRCCS Istituto Ortopedico Galeazzi, Via Galeazzi 4, 20161, Milan, Italy. ·Eur Spine J · Pubmed #29397444.

ABSTRACT: PURPOSE: Most patients suffering from Parkinson's disease (PD) exhibit alterations in the posture, which can in several cases give rise to spine deformities, both in the sagittal and the coronal plane. In addition, degenerative disorders of the spine frequently associated to PD, such as spinal stenosis and sagittal instability, can further impact the quality of life of the patient. In recent years, spine surgery has been increasingly performed, with mixed results. The aim of this narrative review is to analyze the spinal disorders associated to PD, and the current evidence about their surgical treatment. METHODS: Narrative review. RESULTS: Camptocormia, i.e., a pronounced flexible forward bending of the trunk with 7% prevalence, is the most reported sagittal disorder of the spine. Pisa syndrome and scoliosis are both common and frequently associated. Disorders to the spinopelvic alignment were not widely investigated, but a tendency toward a lower ability of PD patients to compensate the sagittal malalignment with respect to non-PD elderly subjects with imbalance seems to emerge. Spine surgery in PD patients showed high rates of complications and re-operations. CONCLUSIONS: Disorders of the posture and spinal alignment, both in the sagittal and in the coronal planes, are common in PD patients, and have a major impact on the quality of life. Outcomes of spine surgery are generally not satisfactory, likely mostly due to muscle dystonia and poor bone quality. Knowledge in this field needs to be consolidated by further clinical and basic science studies. These slides can be retrieved under Electronic Supplementary Material.

15 Review Efficacy and safety of perampanel in Parkinson's disease. A systematic review with meta-analysis. 2018

Lattanzi, Simona / Grillo, Elisabetta / Brigo, Francesco / Silvestrini, Mauro. ·Neurological Clinic, Department of Experimental and Clinical Medicine, Marche Polytechnic University, Via Conca 71, 60020, Ancona, Italy. alfierelattanzisimona@gmail.com. · Medical Department Eisai s.r.l, San Donato Milanese, Italy. · Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. · Division of Neurology, "Franz Tappeiner" Hospital, Merano, BZ, Italy. · Neurological Clinic, Department of Experimental and Clinical Medicine, Marche Polytechnic University, Via Conca 71, 60020, Ancona, Italy. ·J Neurol · Pubmed #29159466.

ABSTRACT: BACKGROUND: L-Dopa represents the mainstay of therapy of Parkinson's disease (PD), but its effectiveness is reduced with continued treatment and disease progression. Accordingly, there remains a need to explore novel treatment strategies to manage the signs and symptoms of the later disease stages. The aim of the study was to evaluate the efficacy and safety of adjunctive perampanel (PER) in patients with PD through a meta-analysis of existing trials. METHODS: Randomized, placebo-controlled, double- or single-blind, add-on studies of PER in patients with PD were identified through a systematic literature search. The following outcomes were assessed: changes from baseline to final efficacy visit in total daily OFF time, activities of daily living during OFF time and motor function during ON time, incidence of adverse events (AEs), and treatment withdrawal. RESULTS: Four trials were included involving 2266 participants, 1449 and 817 for PER and placebo treatment groups, respectively. Four PER daily doses were tested, namely 0.5, 1, 2 and 4 mg. There were no significant differences in any efficacy outcome between PER and placebo treated patients. The risk ratios (RRs) for AEs, severe AEs and treatment withdrawal were similar between placebo and PER at 0.5, 1 and 2 mg; the 4 mg daily dose was associated with an increased risk of AEs [RR 1.118 (1.047-1.193)], and withdrawal for AEs [RR 1.345 (1.034-1.749)] and for any reason [RR 1.197 (1.020-1.406)]. CONCLUSIONS: In PD patients experiencing motor fluctuations, adjunctive PER did not improve the motor state and was well-tolerated at the lower doses.

16 Review Cognitive and behavioral disorders in Parkinson's disease: an update. I: cognitive impairments. 2018

Papagno, Costanza / Trojano, Luigi. ·CIMeC, University of Trento, Trento, Italy. costanza.papagno@unimib.it. · Department of Psychology, University of Milano-Bicocca, Piazza dell'Ateneo 1, 02100, Milan, Italy. costanza.papagno@unimib.it. · Department of Psychology, University of Campania 'Luigi Vanvitelli', Viale Ellittico 31, 81100, Caserta, Italy. luigi.trojano@unicampania.it. · ICS Maugeri, IRCCS, Telese Terme, Italy. luigi.trojano@unicampania.it. ·Neurol Sci · Pubmed #29043468.

ABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by motor symptoms such as rigidity, rest tremor, and bradykinesia. However, a growing body of evidence demonstrated that PD encompasses several non-motor disturbances as well, such as cognitive impairment. Cognitive defects can be present since early stages of the disease but tend to dominate the clinical picture as the disease progresses. Around 40% of patients with PD present with cognitive impairments in several cognitive domains including attention, working memory and executive functions, language, visuospatial skills, and episodic memory; in later stages of the disease, cognitive defects and associated behavioral disorders concur to determine clinically relevant PD-associated dementia. Part of these defects is ascribed to a dopamine-dependent dysfunction of fronto-striatal pathways, but there is a considerable heterogeneity in the cognitive impairments as well as a suggestion of the role of other neurotransmitter systems, such as the cholinergic one, mainly responsible for Parkinson-dementia syndrome. In this paper, we review recent literature with particular attention to the last 5 years on the main cognitive deficits described in PD patients as well as on the hypothesized neuro-functional substrate of such impairments. Finally, we provide some suggestions on how to test cognitive functions in PD appropriately.

17 Review Cognitive and behavioral disorders in Parkinson's disease: an update. II: behavioral disorders. 2018

Trojano, Luigi / Papagno, Costanza. ·Department of Psychology, University of Campania 'Luigi Vanvitelli', Viale Ellittico 31, 81100, Caserta, Italy. luigi.trojano@unicampania.it. · ICS Maugeri, IRCCS, Telese Terme, Italy. luigi.trojano@unicampania.it. · CIMeC, University of Trento, Trento, Italy. costanza.papagno@unimib.it. · Department of Psychology, University of Milano-Bicocca, Piazza dell'Ateneo 1, 02100, Milan, Italy. costanza.papagno@unimib.it. ·Neurol Sci · Pubmed #29038946.

ABSTRACT: Patients with Parkinson's disease (PD) can experience several behavioral symptoms, such as apathy, agitation, hypersexuality, stereotypic movements, pathological gambling, abuse of antiparkinsonian drugs, and REM sleep behavioral disorders. Psychoses and hallucinations, depression and anxiety disorders, and difficulties in recognizing and experiencing emotions also impair behavior and can cause severe psychosocial problems in patients with PD. Symptoms can be present since early stages of the disease, sometimes even before the appearance of classical motor symptoms, likely in relation to dopamine depletion in basal ganglia and/or to dysfunctions of other neurotrasmitter systems, and others can develop later, in some cases in relation to dopaminergic treatment. In this paper, we review recent literature, with particular attention to the last 5 years, on the main behavioral and emotional disturbances described in PD patients as well as the hypothesized neurofunctional substrate of such impairments. Finally, we provide some suggestions on the most suitable instruments to check and assess PD-associated behavioral defects over time.

18 Review Promising rodent models in Parkinson's disease. 2018

Imbriani, Paola / Sciamanna, Giuseppe / Santoro, Massimo / Schirinzi, Tommaso / Pisani, Antonio. ·Neurology, Department of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy; Fondazione Santa Lucia I.R.C.C.S., Laboratory of Neurophysiology and Plasticity, Rome, Italy. · Fondazione Don Gnocchi, Milano, Italy. · Neurology, Department of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy. · Neurology, Department of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy; Fondazione Santa Lucia I.R.C.C.S., Laboratory of Neurophysiology and Plasticity, Rome, Italy. Electronic address: pisani@uniroma2.it. ·Parkinsonism Relat Disord · Pubmed #28760592.

ABSTRACT: BACKGROUND: In the past decade, the study of the pathogenic mechanisms underlying neurodegeneration in Parkinson's disease (PD) has revealed a genetic component, often associated with a number of environmental risk factors. Animal models have improved our understanding of disease pathogenesis, providing significant insights into the understanding of novel molecular pathways. Each model has its own specific features and limitations, and the choice of the most appropriate one depends on the specific question that has to be answered. AIM: To provide an overview of some of the models supporting the hypothesis that early synaptic dysfunction represents a central event in the course of the disease. DEVELOPMENT: Along with "classical" models, based on the administration of neurotoxins and capable of replicating the neuropathological hallmarks of the disease, a number of genetic models, reproducing the disease-causing mutations of monogenic forms of familial PD, have been generated. More recently, novel models have been developed, based on the combination of a toxic insult together with PD mutations, allowing for the identification of dysfunction at a prodromal disease stage. CONCLUSIONS: The development and characterization of new models is crucial for a better understanding of PD related-synaptopathy, and hold promise for the identification of novel therapeutics.

19 Review Modeling the genetic complexity of Parkinson's disease by targeted genome edition in iPS cells. 2017

Calatayud, Carles / Carola, Giulia / Consiglio, Antonella / Raya, Angel. ·Center of Regenerative Medicine in Barcelona (CMRB), Hospital Duran i Reynals, 3rd Floor, Av. Gran Via 199-203, 08908 Hospitalet de Llobregat (Barcelona), Spain; Institute of Biomedicine (IBUB) of the University of Barcelona (UB), 08028 Barcelona, Spain; Department of Pathology and Experimental Therapeutics, School of Medicine, University of Barcelona, 08908 Barcelona, Spain. · Institute of Biomedicine (IBUB) of the University of Barcelona (UB), 08028 Barcelona, Spain; Department of Pathology and Experimental Therapeutics, School of Medicine, University of Barcelona, 08908 Barcelona, Spain. · Institute of Biomedicine (IBUB) of the University of Barcelona (UB), 08028 Barcelona, Spain; Department of Pathology and Experimental Therapeutics, School of Medicine, University of Barcelona, 08908 Barcelona, Spain; Department of Molecular and Translational Medicine, University of Brescia and National Institute of Neuroscience, 25123 Brescia, Italy. Electronic address: aconsiglio@ibub.pcb.ub.es. · Center of Regenerative Medicine in Barcelona (CMRB), Hospital Duran i Reynals, 3rd Floor, Av. Gran Via 199-203, 08908 Hospitalet de Llobregat (Barcelona), Spain; Center for Networked Biomedical Research on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28029 Madrid, Spain; Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010 Barcelona, Spain. Electronic address: araya@cmrb.eu. ·Curr Opin Genet Dev · Pubmed #28759872.

ABSTRACT: Patient-specific iPSC are being intensively exploited as experimental disease models. Even for late-onset diseases of complex genetic influence, such as Parkinson's disease (PD), the use of iPSC-based models is beginning to provide important insights into the genetic bases of PD heritability. Here, we present an update on recently reported genetic risk factors associated with PD. We discuss how iPSC technology, combined with targeted edition of the coding or noncoding genome, can be used to address clinical observations such as incomplete penetrance, and variability in phenoconversion or age-at-onset in familial PD. Finally, we also discuss the relevance of advanced iPSC/CRISPR/Cas9 disease models to ascertain causality in genotype-to-phenotype correlation studies of sporadic PD.

20 Review Treatment of Nonmotor Symptoms in Parkinson's Disease. 2017

Sauerbier, Anna / Cova, Ilaria / Rosa-Grilo, Miguel / Taddei, Raquel N / Mischley, Laurie K / Chaudhuri, K Ray. ·King's College London and King's College Hospital, London, United Kingdom. Electronic address: annasauerbier@nhs.net. · Center for Research and Treatment on Cognitive Dysfunctions, Institute of Clinical Neurology, Luigi Sacco' Hospital, University of Milan, Milan, Italy. · King's College London and King's College Hospital, London, United Kingdom. · Bastyr University Research Institute, Kenmore, WA, United States; UW Graduate Program in Nutritional Sciences, Seattle, WA, United States; University of Washington (UW), Seattle, WA, United States. · National Parkinson Foundation International Centre of Excellence, Kings College and Kings College Hospital, London, United Kingdom; Maurice Wohl Clinical Neuroscience Institute, Kings College, London, United Kingdom; National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre (BRC) and Dementia Unit at South London and Maudsley NHS Foundation Trust, London, United Kingdom. ·Int Rev Neurobiol · Pubmed #28554415.

ABSTRACT: Nonmotor symptoms (NMS) are integral to Parkinson's disease (PD) and the management can often be challenging. In spite of the growing evidence that NMS have a key impact on the quality of life of patients and caregivers, most clinical trials still focus on motor symptoms as primary outcomes. As a consequence strong evidence-based treatment recommendations for NMS occurring in PD are spare. In this chapter, the current data addressing the treatment of major NMS such as sleep, cognitive and autonomic dysfunction, and depression and anxiety are described.

21 Review The many facets of motor learning and their relevance for Parkinson's disease. 2017

Marinelli, Lucio / Quartarone, Angelo / Hallett, Mark / Frazzitta, Giuseppe / Ghilardi, Maria Felice. ·Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Italy. · IRCCS Centro Neurolesi "Bonino-Pulejo", Messina, Department of Neuroscience, University of Messina, Italy; The Fresco Institute for Parkinson's & Movement Disorders, NYU-Langone School of Medicine, New York, NY, USA. · Human Motor Control Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. · Department of Parkinson's Disease and Brain Injury Rehabilitation, "Moriggia-Pelascini" Hospital, Gravedona ed Uniti, Como, Italy. · Department of Physiology, Pharmacology & Neuroscience, CUNY School of Medicine, New York, NY, USA; The Fresco Institute for Parkinson's & Movement Disorders, NYU-Langone School of Medicine, New York, NY, USA. Electronic address: lice.mg79@gmail.com. ·Clin Neurophysiol · Pubmed #28511125.

ABSTRACT: The final goal of motor learning, a complex process that includes both implicit and explicit (or declarative) components, is the optimization and automatization of motor skills. Motor learning involves different neural networks and neurotransmitters systems depending on the type of task and on the stage of learning. After the first phase of acquisition, a motor skill goes through consolidation (i.e., becoming resistant to interference) and retention, processes in which sleep and long-term potentiation seem to play important roles. The studies of motor learning in Parkinson's disease have yielded controversial results that likely stem from the use of different experimental paradigms. When a task's characteristics, instructions, context, learning phase and type of measures are taken into consideration, it is apparent that, in general, only learning that relies on attentional resources and cognitive strategies is affected by PD, in agreement with the finding of a fronto-striatal deficit in this disease. Levodopa administration does not seem to reverse the learning deficits in PD, while deep brain stimulation of either globus pallidus or subthalamic nucleus appears to be beneficial. Finally and most importantly, patients with PD often show a decrease in retention of newly learned skill, a problem that is present even in the early stages of the disease. A thorough dissection and understanding of the processes involved in motor learning is warranted to provide solid bases for effective medical, surgical and rehabilitative approaches in PD.

22 Review Leucine-Rich Repeat Kinase (LRRK2) Genetics and Parkinson's Disease. 2017

Monfrini, Edoardo / Di Fonzo, Alessio. ·IRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Dino Ferrari Center, Neuroscience Section, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. · IRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Dino Ferrari Center, Neuroscience Section, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. alessio.difonzo@policlinico.mi.it. ·Adv Neurobiol · Pubmed #28353276.

ABSTRACT: The discovery of LRRK2 mutations as a cause of Parkinson's disease (PD), including the sporadic late-onset form, established the decisive role of genetics in the field of PD research. Among LRRK2 mutations, the G2019S, mostly lying in a haplotype originating from a common Middle Eastern ancestor, has been identified in different populations worldwide. The G2385R and R1628P variants represent validated risk factors for PD in Asian populations. Here, we describe in detail the origin, the present worldwide epidemiology, and the penetrance of LRRK2 mutations. Furthermore, this chapter aims to characterize other definitely/probably pathogenic mutations and risk variants of LRRK2. Finally, we provide some general guidelines for a LRRK2 genetic testing and counseling. In summary, LRRK2 discovery revolutionized the understanding of PD etiology and laid the foundation for a promising future of genetics in PD research.

23 Review The synaptic function of parkin. 2017

Sassone, Jenny / Serratto, GiuliaMaia / Valtorta, Flavia / Silani, Vincenzo / Passafaro, Maria / Ciammola, Andrea. ·San Raffaele Scientific Institute and Vita-Salute University, Milan, Italy. · CNR Institute of Neuroscience, Department BIOMETRA, Università degli Studi di Milano, Milan, Italy. · IRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Milan, Italy. · Department of Pathophysiology and Transplantation, 'Dino Ferrari' Centre, Università degli Studi di Milano, Milan, Italy. ·Brain · Pubmed #28335015.

ABSTRACT: Loss of function mutations in the gene PARK2, which encodes the protein parkin, cause autosomal recessive juvenile parkinsonism, a neurodegenerative disease characterized by degeneration of the dopaminergic neurons localized in the substantia nigra pars compacta. No therapy is effective in slowing disease progression mostly because the pathogenesis of the disease is yet to be understood. From accruing evidence suggesting that the protein parkin directly regulates synapses it can be hypothesized that PARK2 gene mutations lead to early synaptic damage that results in dopaminergic neuron loss over time. We review evidence that supports the role of parkin in modulating excitatory and dopaminergic synapse functions. We also discuss how these findings underpin the concept that autosomal recessive juvenile parkinsonism can be primarily a synaptopathy. Investigation into the molecular interactions between parkin and synaptic proteins may yield novel targets for pharmacologic interventions.

24 Review Molecular imaging to track Parkinson's disease and atypical parkinsonisms: New imaging frontiers. 2017

Strafella, Antonio P / Bohnen, Nicolaas I / Perlmutter, Joel S / Eidelberg, David / Pavese, Nicola / Van Eimeren, Thilo / Piccini, Paola / Politis, Marios / Thobois, Stephane / Ceravolo, Roberto / Higuchi, Makoto / Kaasinen, Valtteri / Masellis, Mario / Peralta, M Cecilia / Obeso, Ignacio / Pineda-Pardo, Jose Ángel / Cilia, Roberto / Ballanger, Benedicte / Niethammer, Martin / Stoessl, Jon A / Anonymous5120895. ·Morton and Gloria Shulman Movement Disorder Unit & E.J. Safra Parkinson Disease Program, Neurology Div/Dept. Medicine, Toronto Western Hospital, UHN; Krembil Research Institute, UHN; Research Imaging Centre, Campbell Family Mental Health Research Institute, CAMH, University of Toronto, Ontario, Canada. · University of Michigan & Veterans Administration Medical Center, Ann Arbor, Michigan, USA. · Neurology, Radiology, Neuroscience, Physical Therapy & Occupational Therapy, Washington University in St. Louis, St. Louis, Missouri, USA. · Center for Neurosciences, The Feinstein Institute for Medical Research, Manhasset, New York, USA. · Newcastle Magnetic Resonance Centre & Positron Emission Tomography Centre, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne, United Kingdom. · Multimodal Neuroimaging Group-Department of Nuclear Medicine Department of Neurology-University of Cologne, Institute of Neuroscience and Medicine, Jülich Research Center, German Center for Neurodegenerative Diseases (DZNE), Germany. · Neurology Imaging Unit, Centre of Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Hammersmith Campus, Imperial College London, United Kingdom. · Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. · Hospices Civils de Lyon, Hopital Neurologique Pierre Wertheimer, Université Lyon 1; CNRS, Centre de Neurosciences Cognitives, UMR, 5229, Lyon, France. · Department of Clinical and Experimental Medicine, Movement Disorders and Parkinson Center, University of Pisa, Italy. · National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan. · Division of Clinical Neurosciences, Turku University Hospital; Department of Neurology, University of Turku; Turku PET Centre, University of Turku, Turku, Finland. · Cognitive & Movement Disorders Clinic, Sunnybrook Health Sciences Centre; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario, Canada. · Movement Disorder and Parkinson's Disease Program, CEMIC University Hospital, Buenos, Aires, Argentina. · Centro Integral de Neurociencias (CINAC), Hospitales Madrid Puerta del Sur & Centro de Investigación Biomédica en Red, Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. · Parkinson Institute, ASST Gaetano Pini-CTO, Milan, Italy. · INSERM, U1028; CNRS, UMR5292; Lyon Neuroscience Research Center, Neuroplasticity & Neuropathology of Olfactory Perception Team, University Lyon, France. · Pacific Parkinson's Research Centre & National Parkinson Foundation Centre of Excellence, University of British Columbia & Vancouver Coastal Health, Vancouver, British, Columbia, Canada. ·Mov Disord · Pubmed #28150432.

ABSTRACT: Molecular imaging has proven to be a powerful tool for investigation of parkinsonian disorders. One current challenge is to identify biomarkers of early changes that may predict the clinical trajectory of parkinsonian disorders. Exciting new tracer developments hold the potential for in vivo markers of underlying pathology. Herein, we provide an overview of molecular imaging advances and how these approaches help us to understand PD and atypical parkinsonisms. © 2016 International Parkinson and Movement Disorder Society.

25 Review The Contribution of 2017

Longhena, Francesca / Faustini, Gaia / Missale, Cristina / Pizzi, Marina / Spano, PierFranco / Bellucci, Arianna. ·Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. · Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy; IRCCS Fondazione Ospedale San Camillo (NHS-Italy), Venice Lido, Italy. · IRCCS Fondazione Ospedale San Camillo (NHS-Italy), Venice Lido, Italy. ·Neural Plast · Pubmed #28133550.

ABSTRACT: Synaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson's disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onset of motor symptoms that have been related to

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