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Parkinson Disease: HELP
Articles from Michigan
Based on 515 articles published since 2009
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These are the 515 published articles about Parkinson Disease that originated from Michigan during 2009-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
1 Guideline Congress of Neurological Surgeons Systematic Review and Evidence-Based Guideline on Subthalamic Nucleus and Globus Pallidus Internus Deep Brain Stimulation for the Treatment of Patients With Parkinson's Disease: Executive Summary. 2018

Rughani, Anand / Schwalb, Jason M / Sidiropoulos, Christos / Pilitsis, Julie / Ramirez-Zamora, Adolfo / Sweet, Jennifer A / Mittal, Sandeep / Espay, Alberto J / Martinez, Jorge Gonzalez / Abosch, Aviva / Eskandar, Emad / Gross, Robert / Alterman, Ron / Hamani, Clement. ·Neuroscience Institute, Maine Medical Center, Portland, Maine. · Department of Neurosurgery, Henry Ford Medical Gr-oup, West Bloomfield, Michigan. · De-partment of Neurology and Ophthal-mology, Michigan State University, Michigan. · Departments of Neuroscience and Experimental Therapeutics and of Neurosurgery, Albany Medical College, Albany, New York. · Center for Movement Disorders and Neurorestoration, Gain-esville, Florida. · Department of Neuro-surgery, University Hospitals Cleveland Medical Center, Cleveland, Ohio. · De-partment of Neurosurgery, Wayne State University, Detroit, Michigan. · James J. and Joan A. Gardner Center for Parkinson Disease and Movement Disorders, University of Cincinnati, Cincinnati, Ohio. · Neurological Institute, Cleveland Clinic, Cleveland, Ohio. · Department of Neurosurgery, University of Colorado School of Medicine, Aurora, Colorado. · Department of Neurological Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. · Department of Neu-rosurgery, Emory University, Atlanta, Georgia. · Division of Neurosurgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massa-chusetts. · Division of Neurosurgery, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada. ·Neurosurgery · Pubmed #29538685.

ABSTRACT: QUESTION 1: Is bilateral subthalamic nucleus deep brain stimulation (STN DBS) more, less, or as effective as bilateral globus pallidus internus deep brain stimulation (GPi DBS) in treating motor symptoms of Parkinson's disease, as measured by improvements in Unified Parkinson's Disease Rating Scale, part III (UPDRS-III) scores? RECOMMENDATION: Given that bilateral STN DBS is at least as effective as bilateral GPi DBS in treating motor symptoms of Parkinson's disease (as measured by improvements in UPDRS-III scores), consideration can be given to the selection of either target in patients undergoing surgery to treat motor symptoms. (Level I). QUESTION 2: Is bilateral STN DBS more, less, or as effective as bilateral GPi DBS in allowing reduction of dopaminergic medication in Parkinson's disease? RECOMMENDATION: When the main goal of surgery is reduction of dopaminergic medications in a patient with Parkinson's disease, then bilateral STN DBS should be performed instead of GPi DBS. (Level I). QUESTION 3: Is bilateral STN DBS more, less, or as effective as bilateral GPi DBS in treating dyskinesias associated with Parkinson's disease? RECOMMENDATION: There is insufficient evidence to make a generalizable recommendation regarding the target selection for reduction of dyskinesias. However, when the reduction of medication is not anticipated and there is a goal to reduce the severity of "on" medication dyskinesias, the GPi should be targeted. (Level I). QUESTION 4: Is bilateral STN DBS more, less, or as effective as bilateral GPi DBS in improving quality of life measures in Parkinson's disease? RECOMMENDATION: When considering improvements in quality of life in a patient undergoing DBS for Parkinson's disease, there is no basis to recommend bilateral DBS in 1 target over the other. (Level I). QUESTION 5: Is bilateral STN DBS associated with greater, lesser, or a similar impact on neurocognitive function than bilateral GPi DBS in Parkinson disease? RECOMMENDATION: If there is significant concern about cognitive decline, particularly in regards to processing speed and working memory in a patient undergoing DBS, then the clinician should consider using GPi DBS rather than STN DBS, while taking into consideration other goals of surgery. (Level I). QUESTION 6: Is bilateral STN DBS associated with a higher, lower, or similar risk of mood disturbance than GPi DBS in Parkinson's disease? RECOMMENDATION: If there is significant concern about the risk of depression in a patient undergoing DBS, then the clinician should consider using pallidal rather than STN stimulation, while taking into consideration other goals of surgery. (Level I). QUESTION 7: Is bilateral STN DBS associated with a higher, lower, or similar risk of adverse events compared to GPi DBS in Parkinson's disease? RECOMMENDATION: There is insufficient evidence to recommend bilateral DBS in 1 target over the other in order to minimize the risk of surgical adverse events.  The full guideline can be found at: https://www.cns.org/guidelines/deep-brain-stimulation-parkinsons-disease.

2 Editorial Using MRI to Identify Supranuclear Palsy from Parkinson Disease and Dementia with Lewy Bodies. 2019

Shah, Gaurang V. ·From the Department of Radiology, University of Michigan, 1500 E Medical Center Dr, B2A209, Ann Arbor, Mich 48109. ·Radiology · Pubmed #31617819.

ABSTRACT: -- No abstract --

3 Editorial MRIgFUS in tremor-dominant PD does not lead to substantial cognitive adverse events. 2018

Zervos, Thomas M / Hamani, Clement / Schwalb, Jason M. ·From the Department of Neurosurgery (T.M.Z., J.M.S.), Henry Ford Medical Group, Detroit, MI · and Harquail Centre for Neuromodulation (C.H.), Division of Neurosurgery, Sunnybrook Health Science Centre, University of Toronto, Canada. ·Neurology · Pubmed #30158164.

ABSTRACT: -- No abstract --

4 Editorial Translational Research on Stem Cells for Parkinson's Disease. 2018

Parker, Graham C. ·Department of Pediatrics and Children's Hospital of Michigan, Wayne State University School of Medicine , Detroit, Michigan. ·Stem Cells Dev · Pubmed #29995610.

ABSTRACT: -- No abstract --

5 Editorial Challenges in Passive Immunization Strategies to Treat Parkinson Disease. 2018

Manfredsson, Fredric P / Tansey, Malú G / Golde, Todd E. ·Department of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids. · Mercy Health Saint Mary's, Grand Rapids, Michigan. · Department of Physiology, Emory University, Atlanta, Georgia. · McKnight Brain Institute, Center for Translational Research in Neurodegenerative Disease, Department of Neuroscience, University of Florida, Gainesville. ·JAMA Neurol · Pubmed #29913004.

ABSTRACT: -- No abstract --

6 Editorial Cholinergic forebrain density loss in Parkinson disease: More than just cognitive changes. 2018

Bohnen, Nicolaas I / Teipel, Stefan J. ·From the Departments of Radiology (N.I.B.) and Neurology (N.I.B.), University of Michigan · VA Ann Arbor Healthcare System (N.I.B.), MI · German Center for Neurodegenerative Diseases (S.J.T.,) Rostock · and Department of Psychosomatic Medicine (S.J.T.), University of Rostock, Germany. ·Neurology · Pubmed #29618621.

ABSTRACT: -- No abstract --

7 Editorial Alpha-Synuclein to the Rescue: Immune Cell Recruitment by Alpha-Synuclein during Gastrointestinal Infection. 2017

Labrie, Viviane / Brundin, Patrik. ·Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, USA. ·J Innate Immun · Pubmed #28866688.

ABSTRACT: Intraneuronal accumulation of misfolded alpha-synuclein in the central and peripheral nervous systems is strongly linked to Parkinson disease (PD) and other related synucleinopathies. In rare inherited forms of PD, point mutations or gene multiplications mediate the formation of alpha-synuclein protein aggregates. However, in most PD cases it is presumed that the combined effects of ageing and environmental factors drive the formation of alpha-synuclein aggregates. Despite advances regarding alpha-synuclein pathobiology, the normal functions of this protein and factors that regulate its expression are not well understood. We discuss a recent study reporting that viral infection induces alpha-synuclein expression in neurons of the gastrointestinal tract. Alpha-synuclein levels increased during norovirus infection in the duodenum of children. In an in vitro paradigm, monomeric and oligomeric alpha-synuclein acted as chemoattractants for neutrophils and monocytes, and promoted the maturation of dendritic cells. This suggests that alpha-synuclein facilitates immune responses to infection. We explore the possibility that intestinal infections, and associated inflammation, place individuals at increased risk of PD by increasing alpha-synuclein levels and promoting the formation of alpha-synuclein aggregates that propagate in a prion-like fashion via the vagal nerve to the brainstem.

8 Editorial What would Dr. James Parkinson think today? parcelling out the circuitry of levodopa-induced dyskinesias. 2017

Kordower, Jeffrey H. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, 60612. · The Van Andel Research Institute, Grand Rapids Michigan, 49503. ·Mov Disord · Pubmed #28425143.

ABSTRACT: -- No abstract --

9 Editorial What would Dr. James Parkinson think today? II. Neuroimaging in Parkinson's disease. 2017

Albin, Roger L. ·Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. · Neurology Service & Geriatrics Research, Education, and Clinical Center, Veterans Affairs Ann Arbor Health System, Ann Arbor, Michigan, USA. · University of Michigan Morris K. Udall Center of Excellence for Parkinson's Disease Research, Ann Arbor, Michigan, USA. · University of Michigan Alzheimer Disease Center, Ann Arbor, Michigan, USA. ·Mov Disord · Pubmed #28218459.

ABSTRACT: -- No abstract --

10 Editorial Oxidative stress in neurodegenerative disease: causation or association? 2017

Van Raamsdonk, Jeremy M / Vega, Irving E / Brundin, Patrik. ·Laboratory of Aging and Neurodegenerative Disease, Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, USA. · Department of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, MI, USA. · Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, USA. ·Oncotarget · Pubmed #28099897.

ABSTRACT: -- No abstract --

11 Editorial Genetic variation and the D2 dopamine receptor: implications for the treatment of neuropsychiatric disease. 2016

Mickey, Brian J. ·Department of Psychiatry, University of Utah School of Medicine, Salt Lake City, UT, USA. · Department of Psychiatry, University of Michigan Medical School, Ann Arbor, MI, USA. ·Pharmacogenomics · Pubmed #27377823.

ABSTRACT: -- No abstract --

12 Editorial Fetal grafts for Parkinson's disease: Decades in the making. 2016

Kordower, Jeffrey H / Olanow, C Warren. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612; Van Andel Institute, Grand Rapids, MI 49503; jkordowe@rush.edu. · Department of Neurology, Mt. Sinai School of Medicine, New York, NY 10029; Department of Neuroscience, Mt. Sinai School of Medicine, New York, NY 10029. ·Proc Natl Acad Sci U S A · Pubmed #27247420.

ABSTRACT: -- No abstract --

13 Editorial The pharmacodynamics of placebo: expectation effects of price as a proxy for efficacy. 2015

LeWitt, Peter A / Kim, Scott. ·From the Department of Neurology (P.A.L.), Parkinson's Disease and Movement Disorders Center, Henry Ford West Bloomfield Hospital · Department of Neurology (P.A.L.), Wayne State University School of Medicine, Detroit, MI · and Department of Bioethics (S.K.), National Institutes of Health, Bethesda, MD. ·Neurology · Pubmed #25632090.

ABSTRACT: -- No abstract --

14 Editorial How I examine my patient: the art of neurological examination for Parkinson's disease. 2014

Bloem, Bastiaan R / Brundin, Patrik. ·Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Department of Neurology, Nijmegen, The Netherlands. · Laboratory of Translational Parkinson's Disease Research, Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, USA. ·J Parkinsons Dis · Pubmed #25281608.

ABSTRACT: -- No abstract --

15 Editorial Dopamine-dependent functional connectivity in Parkinson disease: a resting-state diagnosis? 2014

Bohnen, Nicolaas I / Martin, W R Wayne. ·From the Departments of Radiology and Neurology (N.I.B.), University of Michigan, and VA Ann Arbor Healthcare System, MI · and the Movement Disorders Program (W.R.W.M.), Division of Neurology, University of Alberta, Edmonton, Canada. ·Neurology · Pubmed #24920849.

ABSTRACT: -- No abstract --

16 Editorial Predicting the development of levodopa-induced dyskinesias: a presynaptic mechanism? 2014

Lewitt, Peter A / Mouradian, M Maral. ·From the Department of Neurology (P.A.L.), Henry Ford Hospital, Bloomfield · the Department of Neurology (P.A.L.), Wayne State University School of Medicine, Detroit, MI · and Center for Neurodegenerative and Neuroimmunologic Diseases (M.M.M.), Department of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ. ·Neurology · Pubmed #24719487.

ABSTRACT: After chronic levodopa use, many patients with Parkinson disease (PD) develop involuntary movements. Whether disabling or minor, levodopa-induced dyskinesia (LID) constitutes an undesirable outcome calling for better treatment strategies. Options for managing LID include delaying its onset by combining a dopaminergic agonist with levodopa from the start(1) or symptomatic control using amantadine. However, fundamental questions about LID remain: by what mechanisms does it develop, and why don't all patients go on to experience LID after sustained levodopa exposure?

17 Editorial Placebo: from belief to movement. 2014

Postuma, Ronald B / Albin, Roger L. ·From the Department of Neurology (R.B.P.), McGill University, Montreal General Hospital, Canada · Neurology Service & GRECC (R.L.A.), VAAAHS · Department of Neurology (R.L.A.), University of Michigan · and Michigan Alzheimer's Disease Center (R.L.A.), Ann Arbor. ·Neurology · Pubmed #24658928.

ABSTRACT: -- No abstract --

18 Editorial Feeling the need ... the need for speed (of processing training) in Parkinson disease. 2013

Chou, Kelvin L / Cronin-Golomb, Alice. ·From the Departments of Neurology and Neurosurgery (K.L.C.), University of Michigan, Ann Arbor · and the Department of Psychology (A.C.-G.), Boston University, MA. ·Neurology · Pubmed #24014502.

ABSTRACT: -- No abstract --

19 Review SLC39A8 gene encoding a metal ion transporter: discovery and bench to bedside. 2019

Nebert, Daniel W / Liu, Zijuan. ·Department of Environmental Health and Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH, 45267-0056, USA. dan.nebert@uc.edu. · Division of Human Genetics, Department of Pediatrics & Molecular Developmental Biology, Cincinnati Children's Hospital, Cincinnati, OH, 45229-2899, USA. dan.nebert@uc.edu. · Department of Biological Sciences, Oakland University, Rochester, MI, 48309, USA. ·Hum Genomics · Pubmed #31521203.

ABSTRACT: SLC39A8 is an evolutionarily highly conserved gene that encodes the ZIP8 metal cation transporter in all vertebrates. SLC39A8 is ubiquitously expressed, including pluripotent embryonic stem cells; SLC39A8 expression occurs in every cell type examined. Uptake of ZIP8-mediated Mn

20 Review Update of the MDS research criteria for prodromal Parkinson's disease. 2019

Heinzel, Sebastian / Berg, Daniela / Gasser, Thomas / Chen, Honglei / Yao, Chun / Postuma, Ronald B / Anonymous3601610. ·Department of Neurology, Christian-Albrechts-University, Kiel, Germany. · Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. · Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, Michigan, USA. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. ·Mov Disord · Pubmed #31412427.

ABSTRACT: The MDS Research Criteria for Prodromal PD allow the diagnosis of prodromal Parkinson's disease using an evidence-based conceptual framework, which was designed to be updated as new evidence becomes available. New prospective evidence of predictive values of risk and prodromal markers published since 2015 was reviewed and integrated into the criteria. Many of the predictive values (likelihood ratios, LR) remain unchanged. The positive likelihood ratio notably increase for olfactory loss and decreased for substantia nigra hyperechogenicity. Negative likelihood ratio remained largely unchanged for all markers. New levels of diagnostic certainty for neurogenic and symptomatic orthostatic hypotension have been added, which substantially differ in positive likelihood ratio from the original publication. For intermediate strength genetic variants, their age-related penetrance is now incorporated in the calculation of the positive likelihood ratio. Moreover, apart from prospective studies, evidence from cross-sectional case-control genome-wide association studies is also considered (given their likely lack of confounding and reverse causation), and to account for the effect of multiple low-penetrance genetic variants polygenic risk scores are added to the model. Diabetes, global cognitive deficit, physical inactivity, and low plasma urate levels in men enter the criteria as new markers. A web-based prodromal PD risk calculator allows the calculation of probabilities of prodromal PD for individuals. Several promising candidate markers may improve the diagnostic accuracy of prodromal PD in the future. © 2019 International Parkinson and Movement Disorder Society.

21 Review Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases. 2019

Espay, Alberto J / Vizcarra, Joaquin A / Marsili, Luca / Lang, Anthony E / Simon, David K / Merola, Aristide / Josephs, Keith A / Fasano, Alfonso / Morgante, Francesca / Savica, Rodolfo / Greenamyre, J Timothy / Cambi, Franca / Yamasaki, Tritia R / Tanner, Caroline M / Gan-Or, Ziv / Litvan, Irene / Mata, Ignacio F / Zabetian, Cyrus P / Brundin, Patrik / Fernandez, Hubert H / Standaert, David G / Kauffman, Marcelo A / Schwarzschild, Michael A / Sardi, S Pablo / Sherer, Todd / Perry, George / Leverenz, James B. ·From the UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders (A.J.E., J.A.V., L.M., A.M.), Department of Neurology, University of Cincinnati, OH · Edmond J. Safra Program in Parkinson's Disease and the Morton and Gloria Shulman Movement Disorders Clinic (A.E.L., A.F.), Toronto Western Hospital, University of Toronto · Krembil Research Institute (A.E.L., A.F.), Toronto, Canada · Parkinson's Disease and Movement Disorders Center (D.K.S.), Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA · College of Medicine (K.A.J.), Mayo Clinic, Rochester, MN · Institute of Molecular and Clinical Sciences (F.M.), St George's University of London, UK · Division of Movement Disorders (R.S.), Department of Neurology and Department of Health Science Research, Mayo Clinic College of Medicine, Rochester, MN · Department of Neurology and the Pittsburgh Institute for Neurodegenerative Diseases (J.T.G., F.C.), University of Pittsburgh, PA · Department of Neurology (T.R.Y.), University of Kentucky, Lexington · Parkinson's Disease Research, Education and Clinical Center (C.M.T.), Neurology, San Francisco Veterans Affairs Medical Center · Department of Neurology (C.M.T.), University of California-San Francisco · Department of Neurology & Neurosurgery, Montreal Neurological Institute, and Department of Human Genetics (Z.G.-O.), McGill University, Canada · Parkinson & Other Movement Disorders Center UC San Diego (I.L.), Department of Neurosciences, Altman Clinical Translational Research Institute, La Jolla, CA · VA Puget Sound Health Care System and Department of Neurology (I.F.M., CP.Z.), University of Washington, Seattle · Department of Neurology (I.F.M.), University of Washington School of Medicine, Seattle · Center for Neurodegenerative Science (P.B.), Van Andel Research Institute, Grand Rapids, MI · Center for Neurological Restoration (H.H.F.) and Lou Ruvo Center for Brain Health, Neurological Institute (J.B.L.), Cleveland Clinic, OH · Department of Neurology (D.G.S.), University of Alabama at Birmingham · Consultorio y Laboratorio de Neurogenética (M.A.K.), Centro Universitario de Neurología "José María Ramos Mejía" y División Neurología, Hospital JM Ramos Mejía, Facultad de Medicina, UBA · Programa de Medicina de Precision y Genomica Clinica (M.A.K.), Instituto de Investigaciones en Medicina Traslacional, Facultad de Ciencias Biomédicas, Universidad Austral-CONICET, Buenos Aires, Argentina · Department of Neurology (M.A.S.), Massachusetts General Hospital, Boston · Division of Neuroscience (S.P.S.), Sanofi-Genzyme, Framingham, MA · Michael J. Fox Foundation for Parkinson's Research (T.S.), New York, NY · and College of Sciences (G.P.), University of Texas at San Antonio. ·Neurology · Pubmed #30745444.

ABSTRACT: The gold standard for a definitive diagnosis of Parkinson disease (PD) is the pathologic finding of aggregated α-synuclein into Lewy bodies and for Alzheimer disease (AD) aggregated amyloid into plaques and hyperphosphorylated tau into tangles. Implicit in this clinicopathologic-based nosology is the assumption that pathologic protein aggregation at autopsy reflects pathogenesis at disease onset. While these aggregates may in exceptional cases be on a causal pathway in humans (e.g., aggregated α-synuclein in

22 Review Triggers, Facilitators, and Aggravators: Redefining Parkinson's Disease Pathogenesis. 2019

Johnson, Michaela E / Stecher, Benjamin / Labrie, Viviane / Brundin, Lena / Brundin, Patrik. ·Center for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Avenue, NE, Grand Rapids, MI 49503, USA; These authors contributed equally to this work. · Tomorrow Edition, Toronto, Canada; These authors contributed equally to this work. · Center for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Avenue, NE, Grand Rapids, MI 49503, USA. · Center for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Avenue, NE, Grand Rapids, MI 49503, USA. Electronic address: Patrik.Brundin@vai.org. ·Trends Neurosci · Pubmed #30342839.

ABSTRACT: We hypothesize that Parkinson's disease (PD) pathogenesis can be divided into three temporal phases. During the first phase, 'triggers', such as viral infections or environmental toxins, spark the disease process in the brain and/or peripheral tissues. Triggers alone, however, may be insufficient, requiring 'facilitators' like peripheral inflammation for PD pathology to develop. Once the disease manifests, 'aggravators' spur further neurodegeneration and exacerbate symptoms. Aggravators are proposed to include impaired autophagy and cell-to-cell propagation of α-synuclein pathology. We believe clinical trials need to consider these three phases and target potential therapies at the appropriate stage of the disease process in order to be effective.

23 Review Quantifying iron content in magnetic resonance imaging. 2019

Ghassaban, Kiarash / Liu, Saifeng / Jiang, Caihong / Haacke, E Mark. ·Magnetic Resonance Innovations, Inc., Bingham Farms, MI, 48025, USA. · The MRI Institute for Biomedical Research, Bingham Farms, MI, 48025, USA. · Shanghai World Foreign Language Academy, Shanghai, China. · Magnetic Resonance Innovations, Inc., Bingham Farms, MI, 48025, USA; The MRI Institute for Biomedical Research, Bingham Farms, MI, 48025, USA; Department of Radiology, Wayne State University, Detroit, MI, 48201, USA. Electronic address: nmrimaging@aol.com. ·Neuroimage · Pubmed #29702183.

ABSTRACT: Measuring iron content has practical clinical indications in the study of diseases such as Parkinson's disease, Huntington's disease, ferritinopathies and multiple sclerosis as well as in the quantification of iron content in microbleeds and oxygen saturation in veins. In this work, we review the basic concepts behind imaging iron using T2, T2*, T2', phase and quantitative susceptibility mapping in the human brain, liver and heart, followed by the applications of in vivo iron quantification in neurodegenerative diseases, iron tagged cells and ultra-small superparamagnetic iron oxide (USPIO) nanoparticles.

24 Review Imaging Markers of Progression in Parkinson's Disease. 2018

Strafella, Antonio P / Bohnen, Nico I / Pavese, Nicola / Vaillancourt, David E / van Eimeren, Thilo / Politis, Marios / Tessitore, Alessandro / Ghadery, Christine / Lewis, Simon / Anonymous1461606. ·Morton and Gloria Shulman Movement Disorder Unit & E.J. Safra Parkinson Disease Program, Neurology Division, Department of Medicine, Toronto Western Hospital, UHN University of Toronto Toronto Ontario Canada. · Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Research Institute, UHN University of Toronto Toronto Ontario Canada. · Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health University of Toronto Toronto Ontario Canada. · Department of Radiology & Neurology University of Michigan Ann Arbor Michigan USA. · Veterans Administration Ann Arbor Healthcare System Ann Arbor Michigan USA. · Morris K. Udall Center of Excellence for Parkinson's Disease Research University of Michigan Ann Arbor Michigan USA. · Newcastle Magnetic Resonance Centre & Positron Emission Tomography Centre Newcastle University, Campus for Ageing & Vitality Newcastle upon Tyne United Kingdom. · Applied Physiology and Kinesiology, Biomedical Engineering, and Neurology University of Florida Gainesville Florida USA. · Department of Nuclear Medicine and Department of Neurology University of Cologne Cologne Germany. · Institute for Cognitive Neuroscience, Jülich Research Centre Jülich Germany. · German Center for Neurodegenerative Diseases (DZNE) Bonn-Cologne Bonn Germany. · Neurodegeneration Imaging Group (NIG), Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London London United Kingdom. · Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences-MRI Research Center SUN-FISM University of Campania "Luigi Vanvitelli" Naples Italy. · Parkinson's Disease Research Clinic, Brain and Mind Centre University of Sydney Sydney NSW Australia. ·Mov Disord Clin Pract · Pubmed #30637278.

ABSTRACT: Background: Parkinson's disease (PD) is the second-most common neurodegenerative disorder after Alzheimer's disease; however, to date, there is no approved treatment that stops or slows down disease progression. Over the past decades, neuroimaging studies, including molecular imaging and MRI are trying to provide insights into the mechanisms underlying PD. Methods: This work utilized a literature review. Results: It is now becoming clear that these imaging modalities can provide biomarkers that can objectively detect brain changes related to PD and monitor these changes as the disease progresses, and these biomarkers are required to establish a breakthrough in neuroprotective or disease-modifying therapeutics. Conclusions: Here, we provide a review of recent observations deriving from PET, single-positron emission tomography, and MRI studies exploring PD and other parkinsonian disorders.

25 Review The Search for Environmental Causes of Parkinson's Disease: Moving Forward. 2018

Chen, Honglei / Ritz, Beate. ·Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, MI, USA. · Department of Epidemiology and Environmental Health Sciences, Fielding School of Public Health, University of California Los Angeles, Los Angeles, CA, USA. ·J Parkinsons Dis · Pubmed #30584168.

ABSTRACT: It is widely believed that environmental exposures contribute to the vast majority of late-onset sporadic Parkinson's disease (PD), alone or via interactions with genetic factors. The search for environmental causes of PD has however been hampered by lack of understanding the prodromal phase of PD development and the difficulties in exposure assessment during this prolonged period. On the other hand, the existence of this prodromal period, along with an increasingly better understanding of PD prodromal symptoms, provides an exciting opportunity to identify environmental factors that initiate PD pathogenesis and/or modify its progression. For prevention efforts, this prodromal stage is of a major interest. Targeting factors that enter the body via the nose or gut has become even more important since the discovery of α-synuclein aggregates in the enteric and olfactory nervous systems. In this paper, we speculate about novel research hypotheses and approaches that may help us better define the role of environment in PD etiology, especially during its extended and complex prodromal phase.

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