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Parkinson Disease: HELP
Articles from New York
Based on 971 articles published since 2008
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These are the 971 published articles about Parkinson Disease that originated from New York 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 When to Start Levodopa Therapy for Parkinson's Disease. 2019

Bressman, Susan / Saunders-Pullman, Rachel. ·From the Icahn School of Medicine at Mt. Sinai, New York. ·N Engl J Med · Pubmed #30673551.

ABSTRACT: -- No abstract --

2 Editorial Translating scientific advances into disease-modifying therapies for Parkinson's Disease. 2017

Cenci, M Angela / Olanow, C Warren. ·Basal Ganglia Pathophysiology Unit, Dept. Exp. Med. Science, Lund University, Lund (Sweden). · Clintrex LLC; Department of Neurology and Department of Neurosciences, Mount Sinai School of Medicine, New York. ·Exp Neurol · Pubmed #29145992.

ABSTRACT: -- No abstract --

3 Editorial Understanding of the role of manganese in parkinsonism and Parkinson disease. 2017

Ratner, Marcia H / Fitzgerald, Edward. ·From the Laboratory of Molecular Neurobiology (M.H.R.), Department of Pharmacology & Experimental Therapeutics, Boston University School of Medicine, MA · and Department of Environmental Health Sciences (E.F.), School of Public Health, University at Albany, Rensselaer, NY. ·Neurology · Pubmed #28031391.

ABSTRACT: -- No abstract --

4 Editorial Nanomedicine in brain repair: Alzheimer's, Parkinson's and the proteome. 2017

Broderick, Patricia A / Jacoby, Jacob H. ·City University of New York School of Medicine, Sophie Davis School of Biomedical Education, City College of New York, 160 Convent Ave., New York, NY, 10031, USA. broderick@med.cuny.com. · , Mailroom, Harris Hall Rm 01, New York, USA. broderick@med.cuny.com. · NYU Langone Medical Center, Comprehensive Epilepsy Center, 560 First Ave., New York, NY, 10016, USA. broderick@med.cuny.com. · Rutgers Medical School, Newark, NJ, USA. · Bayonne Medical Center, Bayonne, NJ, USA. ·J Neural Transm (Vienna) · Pubmed #28028642.

ABSTRACT: -- No abstract --

5 Editorial Orthostatic hypotension, cognition, and Parkinson disease: Dumbing down by standing up. 2017

Boylan, Laura S / Messinis, Lambros. ·From the Department of Neurology (L.S.B.), New York University School of Medicine, New York · Department of Neurology (L.S.B.), Essentia Health, Duluth, MN · Department of Neurology (L.S.B.), Bellevue Hospital, New York, NY · and Neuropsychology Section, Department of Neurology (L.M.), University of Patras Medical School, Greece. ·Neurology · Pubmed #27903812.

ABSTRACT: -- No abstract --

6 Editorial Cytokines as Potential Biomarkers of Parkinson Disease. 2016

Alcalay, Roy N. ·Department of Neurology, College of Physicians and Surgeons, Columbia University Medical Center, New York, New York2Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University Medical Center, New York, New York. ·JAMA Neurol · Pubmed #27669063.

ABSTRACT: -- No abstract --

7 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 --

8 Editorial Advances in Experimental Neuropathology: New Methods and Insights. 2016

Roth, Kevin A. ·Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York. Electronic address: karoth@columbia.edu. ·Am J Pathol · Pubmed #26802320.

ABSTRACT: This Editorial introduces this month's special Neuropathology Theme Issue, a series of Reviews on advances in our understanding of rare human hereditary neuropathies, peripheral nervous system tumors, and common degenerative diseases.

9 Editorial Eldad Melamed 1942-2015: Ave atque--A memorial. 2016

Olanow, C Warren / Poewe, Werner. ·Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA. · Medical University Innsbruck, Innsbruck, Austria. ·Mov Disord · Pubmed #26685050.

ABSTRACT: -- No abstract --

10 Editorial Milk consumption and the risk of nigral degeneration. 2016

Chen, Honglei / Marder, Karen. ·From the Epidemiology Branch (H.C.), National Institute of Environmental Health Sciences, Research Triangle Park, NC · and the Department of Neurology (K.M.), College of Physicians and Surgeons, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY. ·Neurology · Pubmed #26658908.

ABSTRACT: -- No abstract --

11 Editorial Levodopa: 50 years of a revolutionary drug for Parkinson disease. 2015

Fahn, Stanley / Poewe, Werner. ·Columbia University College of Physicians and Surgeons, 710 West 168th Street, New York, NY, 10032, U.S.A. ·Mov Disord · Pubmed #25488146.

ABSTRACT: -- No abstract --

12 Editorial Peripheral alpha-synuclein and Parkinson's disease. 2014

Olanow, C Warren / Wakeman, Dustin R / Kordower, Jeffrey H. ·Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY, 10029, USA. ·Mov Disord · Pubmed #25043799.

ABSTRACT: -- No abstract --

13 Editorial Sex differences in neurological and psychiatric disorders. 2014

Young, Larry J / Pfaff, Donald W. ·Center for Translational Social Neuroscience, Department of Psychiatry and Behavioral Sciences, Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, United States. Electronic address: lyoun03@emory.edu. · Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY 10021, United States. ·Front Neuroendocrinol · Pubmed #24882637.

ABSTRACT: -- No abstract --

14 Editorial Freezing of gait in PD has a REM correlate: twice cursed with a shared pathophysiology? 2013

Hershey, Linda A / Lichter, David G. ·From the Department of Neurology (L.A.H.), University of Oklahoma Health Sciences Center, Oklahoma City · Department of Neurology (D.G.L.), University at Buffalo School of Medicine (SUNY), NY · and Veterans Affairs Western New York Healthcare System (D.G.L.), Buffalo. ·Neurology · Pubmed #23946300.

ABSTRACT: -- No abstract --

15 Editorial Discovering neuroprotection in Parkinson's disease, or getting to haphazard. 2010

Kieburtz, Karl. ·University of Rochester Medical Center, Rochester, NY, USA. karl.kieburtz@ctcc.rochester.edu ·Mt Sinai J Med · Pubmed #21105130.

ABSTRACT: Despite significant research efforts, a therapy to slow or halt the progression of Parkinson's disease ("neuroprotection") remains elusive. The discovery of such a therapy will likely require important observations from a number of perspectives: basic science investigation, clinical research, and careful observation in medical practice. Any possible insights will require confirmation in rigorous clinical trial testing. Combining the useful insights from all perspectives may be the most promising approach to discovering a neuroprotective therapy.

16 Editorial A critical evaluation of the Braak staging scheme for Parkinson's disease. 2008

Burke, Robert E / Dauer, William T / Vonsattel, Jean Paul G. ·Department of Neurology, Columbia University Medical Center, New York, NY, USA. rb43@columbia.edu ·Ann Neurol · Pubmed #19067353.

ABSTRACT: Braak and colleagues have proposed that, within the central nervous system, Parkinson's disease (PD) begins as a synucleinopathy in nondopaminergic structures of the lower brainstem or in the olfactory bulb. The brainstem synucleinopathy is postulated to progress rostrally to affect the substantia nigra and cause parkinsonism at a later stage of the disease. In the context of a diagnosis of PD, made from current clinical criteria, the pattern of lower brainstem involvement accompanying mesencephalic synucleinopathy is often observed. However, outside of that context, the patterns of synucleinopathy that Braak described are often not observed, particularly in dementia with Lewy bodies and when synucleinopathy occurs in the absence of neurological manifestations. The concept that lower brainstem synucleinopathy represents "early PD" rests on the supposition that it has a substantial likelihood of progressing within the human lifetime to involve the mesencephalon, and thereby cause the substantia nigra pathology and clinical parkinsonism that have heretofore defined the disease. However, the predictive validity of this concept is doubtful, based on numerous observations made in populations of aged individuals who, despite the absence of neurological signs, have brain synucleinopathy ranging up to Braak stages 4 to 6 at postmortem. Furthermore, there is no relation between Braak stage and the clinical severity of PD. We conclude that the relation between patterns of abnormal synuclein immunostaining in the human brain and the disease entity now recognized as PD remains to be determined.

17 Review Functional and behavioral consequences of Parkinson's disease-associated 2018

Benson, Deanna L / Matikainen-Ankney, Bridget A / Hussein, Ayan / Huntley, George W. ·Department of Neuroscience, Friedman Brain Institute, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, U.S.A. deanna.benson@mssm.edu. · Department of Neuroscience, Friedman Brain Institute, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, U.S.A. ·Biochem Soc Trans · Pubmed #30514770.

ABSTRACT:

18 Review Alterations of Expression of the Serotonin 5-HT4 Receptor in Brain Disorders. 2018

Rebholz, Heike / Friedman, Eitan / Castello, Julia. ·Department of Molecular, Cellular and Biomedical Sciences, CUNY School of Medicine, New York, NY 10031, USA. heikerebholz@gmail.com. · Department of Molecular, Cellular and Biomedical Sciences, CUNY School of Medicine, New York, NY 10031, USA. Friedman@med.cuny.edu. · Ph.D. Programs in Biochemistry and Biology, The Graduate Center, City University of New York, New York, NY 10031, USA. Friedman@med.cuny.edu. · Department of Molecular, Cellular and Biomedical Sciences, CUNY School of Medicine, New York, NY 10031, USA. julia.csaval@gmail.com. · Ph.D. Programs in Biochemistry and Biology, The Graduate Center, City University of New York, New York, NY 10031, USA. julia.csaval@gmail.com. ·Int J Mol Sci · Pubmed #30428567.

ABSTRACT: The serotonin 4 receptor, 5-HT₄R, represents one of seven different serotonin receptor families and is implicated in a variety of physiological functions and their pathophysiological variants, such as mood and depression or anxiety, food intake and obesity or anorexia, or memory and memory loss in Alzheimer's disease. Its central nervous system expression pattern in the forebrain, in particular in caudate putamen, the hippocampus and to lesser extent in the cortex, predispose it for a role in executive function and reward-related actions. In rodents, regional overexpression or knockdown in the prefrontal cortex or the nucleus accumbens of 5-HT₄R was shown to impact mood and depression-like phenotypes, food intake and hypophagia; however, whether expression changes are causally involved in the etiology of such disorders is not clear. In this context, more data are emerging, especially based on PET technology and the use of ligand tracers that demonstrate altered 5-HT₄R expression in brain disorders in humans, confirming data stemming from post-mortem tissue and preclinical animal models. In this review, we would like to present the current knowledge of 5-HT₄R expression in brain regions relevant to mood/depression, reward and executive function with a focus on 5-HT₄R expression changes in brain disorders or caused by drug treatment, at both the transcript and protein levels.

19 Review Network imaging biomarkers: insights and clinical applications in Parkinson's disease. 2018

Schindlbeck, Katharina A / Eidelberg, David. ·Center for Neurosciences, The Feinstein Institute for Medical Research, Manhasset, NY, USA. · Center for Neurosciences, The Feinstein Institute for Medical Research, Manhasset, NY, USA. Electronic address: deidelbe@northwell.edu. ·Lancet Neurol · Pubmed #29914708.

ABSTRACT: Parkinson's disease presents several practical challenges: it can be difficult to distinguish from atypical parkinsonian syndromes, clinical ratings can be insensitive as markers of disease progression, and its non-motor manifestations are not readily assessed in animal models. These challenges, along with others, are beginning to be addressed by innovative imaging methods to characterise Parkinson's disease-specific functional networks across the whole brain and measure their expression in each patient. These signatures can help improve differential diagnosis, guide selection of patients for clinical trials, and quantify treatment responses and placebo effects in individual patients. The primary Parkinson's disease-related metabolic pattern has been replicated in multiple patient populations and used as an outcome measure in clinical trials. It can also be used as a predictor of near-term phenoconversion in prodromal syndromes, such as rapid eye movement sleep behaviour disorder. Functional network imaging holds great promise for future clinical use in the management of neurodegenerative disorders.

20 Review A new outlook on cholinergic interneurons in Parkinson's disease and L-DOPA-induced dyskinesia. 2018

Conti, Melissa M / Chambers, Nicole / Bishop, Christopher. ·Behavioral Neuroscience Program, Department of Psychology, Binghamton University, 4400 Vestal Parkway East, Binghamton, NY 13902-6000, USA. Electronic address: mconti2@binghamton.edu. · Behavioral Neuroscience Program, Department of Psychology, Binghamton University, 4400 Vestal Parkway East, Binghamton, NY 13902-6000, USA. Electronic address: nchambe4@binghamton.edu. · Behavioral Neuroscience Program, Department of Psychology, Binghamton University, 4400 Vestal Parkway East, Binghamton, NY 13902-6000, USA. Electronic address: cbishop@binghamton.edu. ·Neurosci Biobehav Rev · Pubmed #29782883.

ABSTRACT: Traditionally, dopamine (DA) and acetylcholine (ACh) striatal systems were considered antagonistic and imbalances or aberrant signaling between these neurotransmitter systems could be detrimental to basal ganglia activity and pursuant motor function, such as in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID). Herein, we discuss the involvement of cholinergic interneurons (ChIs) in striatally-mediated movement in a healthy, parkinsonian, and dyskinetic state. ChIs integrate numerous neurotransmitter signals using intrinsic glutamate, serotonin, and DA receptors and convey the appropriate transmission onto nearby muscarinic and nicotinic ACh receptors to produce movement. In PD, severe DA depletion causes abnormal rises in ChI activity which promote striatal signaling to attenuate normal movement. When treating PD with L-DOPA, hyperkinetic side effects, or LID, develop due to increased striatal DA; however, the role of ChIs and ACh transmission, until recently has been unclear. Fortunately, new technology and pharmacological agents have facilitated understanding of ChI function and ACh signaling in the context of LID, thus offering new opportunities to modify existing and discover future therapeutic strategies in movement disorders.

21 Review Sleep disorders and Parkinson disease; lessons from genetics. 2018

Gan-Or, Ziv / Alcalay, Roy N / Rouleau, Guy A / Postuma, Ronald B. ·Montreal Neurological Institute, McGill University, Montréal, QC, Canada; Department of Human Genetics, McGill University, Montréal, QC, Canada; Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. Electronic address: ziv.gan-or@mail.mcgill.ca. · Department of Neurology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, NY, USA. · Montreal Neurological Institute, McGill University, Montréal, QC, Canada; Department of Human Genetics, McGill University, Montréal, QC, Canada; Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. · Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. ·Sleep Med Rev · Pubmed #29449121.

ABSTRACT: Parkinson disease is a common, age-related neurodegenerative disorder, projected to afflict millions of individuals in the near future. Understanding its etiology and identifying clinical, genetic or biological markers for Parkinson disease onset and progression is therefore of major importance. Various sleep-related disorders are the most common group of non-motor symptoms in advanced Parkinson disease, but they can also occur during its prodromal phase. However, with the exception of REM sleep behavior disorder, it is unclear whether they are part of the early pathological process of Parkinson disease, or if they develop as Parkinson disease advances because of treatments and neurodegeneration progression. The advancements in genetic studies in the past two decades have generated a wealth of information, and recent genetic studies offer new insight on the association of sleep-related disorders with Parkinson disease. More specifically, comparing genetic data between Parkinson disease and sleep-related disorders can clarify their association, which may assist in determining whether they can serve as clinical markers for Parkinson disease risk or progression. In this review, we discuss the current knowledge on the genetics of sleep-related disorders in Parkinson disease context, and the potential implications on research, diagnosis, counseling and treatment.

22 Review Synaptic plasticity may underlie l-DOPA induced dyskinesia. 2018

Borgkvist, Anders / Lieberman, Ori J / Sulzer, David. ·Departments of Neurology, Columbia University Medical Center and Division of Molecular Therapeutics, New York State Psychiatric Institute, United States. Electronic address: ab3380@cumc.columbia.edu. · Departments of Psychiatry, Pharmacology, Columbia University Medical Center and Division of Molecular Therapeutics, New York State Psychiatric Institute, United States. ·Curr Opin Neurobiol · Pubmed #29125979.

ABSTRACT: l-DOPA provides highly effective treatment for Parkinson's disease, but l-DOPA induced dyskinesia (LID) is a very debilitating response that eventually is presented by a majority of patients. A central issue in understanding the basis of LID is whether it is due to a response to chronic l-DOPA over years of therapy, and/or due to synaptic changes that follow the loss of dopaminergic neurotransmission and then triggered by acute l-DOPA administration. We review recent work that suggests that specific synaptic changes in the D1 dopamine receptor-expressing direct pathway striatal projection neurons due to loss of dopamine in Parkinson's disease are responsible for LID. Chronic l-DOPA may nevertheless modulate LID through priming mechanisms.

23 Review Diagnosis of multiple system atrophy. 2018

Palma, Jose-Alberto / Norcliffe-Kaufmann, Lucy / Kaufmann, Horacio. ·Department of Neurology, Dysautonomia Center, New York University School of Medicine, NY, USA. · Department of Neurology, Dysautonomia Center, New York University School of Medicine, NY, USA. Electronic address: Horacio.Kaufmann@nyumc.org. ·Auton Neurosci · Pubmed #29111419.

ABSTRACT: Multiple system atrophy (MSA) may be difficult to distinguish clinically from other disorders, particularly in the early stages of the disease. An autonomic-only presentation can be indistinguishable from pure autonomic failure. Patients presenting with parkinsonism may be misdiagnosed as having Parkinson disease. Patients presenting with the cerebellar phenotype of MSA can mimic other adult-onset ataxias due to alcohol, chemotherapeutic agents, lead, lithium, and toluene, or vitamin E deficiency, as well as paraneoplastic, autoimmune, or genetic ataxias. A careful medical history and meticulous neurological examination remain the cornerstone for the accurate diagnosis of MSA. Ancillary investigations are helpful to support the diagnosis, rule out potential mimics, and define therapeutic strategies. This review summarizes diagnostic investigations useful in the differential diagnosis of patients with suspected MSA. Currently used techniques include structural and functional brain imaging, cardiac sympathetic imaging, cardiovascular autonomic testing, olfactory testing, sleep study, urological evaluation, and dysphagia and cognitive assessments. Despite advances in the diagnostic tools for MSA in recent years and the availability of consensus criteria for clinical diagnosis, the diagnostic accuracy of MSA remains sub-optimal. As other diagnostic tools emerge, including skin biopsy, retinal biomarkers, blood and cerebrospinal fluid biomarkers, and advanced genetic testing, a more accurate and earlier recognition of MSA should be possible, even in the prodromal stages. This has important implications as misdiagnosis can result in inappropriate treatment, patient and family distress, and erroneous eligibility for clinical trials of disease-modifying drugs.

24 Review Hepatitis C virus infection and risk of Parkinson's disease: a systematic review and meta-analysis. 2018

Wijarnpreecha, Karn / Chesdachai, Supavit / Jaruvongvanich, Veeravich / Ungprasert, Patompong. ·Department of Internal Medicine, Bassett Medical Center, Cooperstown, New York. · Department of Medicine, Faculty of Medicine Ramathibodi Hospital. · Department of Internal Medicine, University of Hawaii, Honolulu, Hawaii. · Department of Internal Medicine, Division of Rheumatology, Mayo Clinic, Rochester, Minnesota, USA. · Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. ·Eur J Gastroenterol Hepatol · Pubmed #29049127.

ABSTRACT: BACKGROUND/OBJECTIVE: Hepatitis C virus (HCV) infection is one of the most common infections worldwide. Recent epidemiologic studies have suggested that patients with HCV infection might be at an increased risk of Parkinson's disease. However, the data on this relationship remain inconclusive. This meta-analysis was conducted with the aim to summarize all available evidence. PATIENTS AND METHODS: A literature search was performed using MEDLINE and EMBASE database from inception to May 2017. Studies that reported relative risks, odd ratios (ORs), or hazard ratios comparing the risk of Parkinson's disease among HCV-infected patients versus participants without HCV infection were included. Pooled OR and 95% confidence interval were calculated using a random-effect, generic inverse variance method. RESULTS: Of 468 studies, five studies with 323 974 participants met our eligibility criteria and were included in the analysis. We found a higher risk of Parkinson's disease among patients with chronic HCV infection compared with participants without HCV infection with the pooled OR of 1.35 (95% confidence interval: 1.19-1.52). The statistical heterogeneity of this study was insignificant (I=3%). The main limitation of this meta-analysis was the limited accuracy of diagnosis in the primary studies as they were coding-based studies. CONCLUSION: This study demonstrated a higher risk of Parkinson's disease among HCV-infected patients. Further studies are required to clarify how this risk should be addressed in the clinical picture.

25 Review The 200-year journey of Parkinson disease: Reflecting on the past and looking towards the future. 2018

Fahn, Stanley. ·Columbia University College of Physicians and Surgeons, 710 West 168th Street, New York, NY 10032, USA. Electronic address: sf1@columbia.edu. ·Parkinsonism Relat Disord · Pubmed #28784297.

ABSTRACT: It took almost 100 years before a meaningful advance occurred in any basic science understanding of Parkinson disease (PD) following James Parkinson's description in 1817. The Lewy body was described in 1912, and the substantia nigra was found to be depigmented with neuronal loss and gliosis in 1919. The link between dopamine and PD began in 1957, 140 years after Parkinson's Essay. Arvid Carlsson and Oleh Hornykiewicz were the major pioneers. The revolutionary therapeutic breakthrough was the introduction of high dosage levodopa therapy by George Cotzias in 1967. Following 40 years of the dopa/dopamine era, we have entered the era of alpha-synuclein, the protein present in Lewy bodies. Heiko Braak found that alpha-synuclein accumulates initially in the olfactory system and lower brainstem and then travels in an anatomic pattern to involve other regions of the brain and thereby cause progressive symptoms. Alpha-synuclein was somehow converted to a rogue protein. Where this originates and how it is propagated are under intense investigation. At the same time that the alpha-synuclein era was developing, clinical advances took place by recognizing PD as hosting a wide variety of nonmotor features with eventual cognitive impairment in many. Therapeutics has also evolved. Although the most effective therapy for the motor features remains levodopa, surgical approaches and drugs for nonmotor problems continue to expand our ability to treat people with PD. We can expect therapeutic advances in neuroprotection as the basic science discoveries uncovered in the alpha-synuclein era are translated into effective treatments.

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