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Jay S. Schneider

Bio: Jay S. Schneider is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: MPTP & Parkinson's disease. The author has an hindex of 41, co-authored 142 publications receiving 9820 citations. Previous affiliations of Jay S. Schneider include University of Rochester Medical Center.


Papers
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Journal ArticleDOI
Christopher G. Goetz1, Barbara C. Tilley2, Stephanie R. Shaftman2, Glenn T. Stebbins1, Stanley Fahn3, Pablo Martinez-Martin, Werner Poewe4, Cristina Sampaio5, Matthew B. Stern6, Richard Dodel7, Bruno Dubois8, Robert G. Holloway9, Joseph Jankovic10, Jaime Kulisevsky11, Anthony E. Lang12, Andrew J. Lees13, Sue Leurgans1, Peter A. LeWitt14, David L. Nyenhuis15, C. Warren Olanow16, Olivier Rascol17, Anette Schrag13, Jeanne A. Teresi3, Jacobus J. van Hilten18, Nancy R. LaPelle19, Pinky Agarwal, Saima Athar, Yvette Bordelan, Helen Bronte-Stewart, Richard Camicioli, Kelvin L. Chou, Wendy Cole, Arif Dalvi, Holly Delgado, Alan Diamond, Jeremy P.R. Dick, John E. Duda, Rodger J. Elble, Carol Evans, V. G. H. Evidente, Hubert H. Fernandez, Susan H. Fox, Joseph H. Friedman, Robin D. Fross, David A. Gallagher, Deborah A. Hall, Neal Hermanowicz, Vanessa K. Hinson, Stacy Horn, Howard I. Hurtig, Un Jung Kang, Galit Kleiner-Fisman, Olga Klepitskaya, Katie Kompoliti, Eugene C. Lai, Maureen L. Leehey, Iracema Leroi, Kelly E. Lyons, Terry McClain, Steven W. Metzer, Janis M. Miyasaki, John C. Morgan, Martha Nance, Joanne Nemeth, Rajesh Pahwa, Sotirios A. Parashos, Jay S. Schneider, Kapil D. Sethi, Lisa M. Shulman, Andrew Siderowf, Monty Silverdale, Tanya Simuni, Mark Stacy, Robert Malcolm Stewart, Kelly L. Sullivan, David M. Swope, Pettaruse M. Wadia, Richard Walker, Ruth H. Walker, William J. Weiner, Jill Wiener, Jayne R. Wilkinson, Joanna M. Wojcieszek, Summer C. Wolfrath, Frederick Wooten, Allen Wu, Theresa A. Zesiewicz, Richard M. Zweig 
TL;DR: The combined clinimetric results of this study support the validity of the MDS‐UPDRS for rating PD.
Abstract: We present a clinimetric assessment of the Movement Disorder Society (MDS)-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). The MDS-UDPRS Task Force revised and expanded the UPDRS using recommendations from a published critique. The MDS-UPDRS has four parts, namely, I: Non-motor Experiences of Daily Living; II: Motor Experiences of Daily Living; III: Motor Examination; IV: Motor Complications. Twenty questions are completed by the patient/caregiver. Item-specific instructions and an appendix of complementary additional scales are provided. Movement disorder specialists and study coordinators administered the UPDRS (55 items) and MDS-UPDRS (65 items) to 877 English speaking (78% non-Latino Caucasian) patients with Parkinson's disease from 39 sites. We compared the two scales using correlative techniques and factor analysis. The MDS-UPDRS showed high internal consistency (Cronbach's alpha = 0.79-0.93 across parts) and correlated with the original UPDRS (rho = 0.96). MDS-UPDRS across-part correlations ranged from 0.22 to 0.66. Reliable factor structures for each part were obtained (comparative fit index > 0.90 for each part), which support the use of sum scores for each part in preference to a total score of all parts. The combined clinimetric results of this study support the validity of the MDS-UPDRS for rating PD.

4,589 citations

Journal ArticleDOI
01 Jan 2003-Brain
TL;DR: The present review discusses the current state of knowledge concerning the effects of lead on the cognitive development of children, and suggests that there are toxicological effects with behavioural concomitants at exceedingly low levels of exposure.
Abstract: Lead has been recognized as a poison for millennia and has been the focus of public health regulation in much of the developed world for the better part of the past century. The nature of regulation has evolved in response to increasing information provided by vigorous scientific investigation of lead's effects. In recognition of the particular sensitivity of the developing brain to lead's pernicious effects, much of this legislation has been addressed to the prevention of childhood lead poisoning. The present review discusses the current state of knowledge concerning the effects of lead on the cognitive development of children. Addressed are the reasons for the child's exquisite sensitivity, the behavioural effects of lead, how these effects are best measured, and the long-term outlook for the poisoned child. Of particular importance are the accumulating data suggesting that there are toxicological effects with behavioural concomitants at exceedingly low levels of exposure. In addition, there is also evidence that certain genetic and environmental factors can increase the detrimental effects of lead on neural development, thereby rendering certain children more vulnerable to lead neurotoxicity. The public health implications of these findings are discussed.

976 citations

Journal ArticleDOI
TL;DR: A review of recent developments in the understanding of the transport of manganese (Mn) into the central nervous system (CNS), as well as brain imaging and neurocognitive studies in non-human primates aimed at improving the mechanisms of Mn neurotoxicity is presented in this article.

541 citations

Journal ArticleDOI
TL;DR: Critical assessment of animal models shows that chronic low‐dose MPTP treatment in primates recapitulates PD‐MCI over time, enhancing the current biological concept of PD‐ MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems.
Abstract: The recent formalization of clinical criteria for Parkinson's disease with dementia (PDD) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PDD occurs on the background of severe dopamine deficits with, the main pathological drivers of cognitive decline being a synergistic effect between alpha-synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin, and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α-synuclein gene, lead to a clear increased risk of PDD, whereas others, such as parkin mutations, are associated with a reduced risk of PDD. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low-dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. Whereas dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies, and genetic factors in PD-MCI remains to be fully elucidated.

292 citations

Journal ArticleDOI
Karl Kieburtz1, Bernard Ravina2, Bernard Ravina1, Wendy R. Galpern2, Barbara C. Tilley3, Kathleen M. Shannon4, Caroline M. Tanner, G. Frederick Wooten5, Robert W. Hamill6, Jacob I. Sage7, Emily Kosa7, Ray L. Watts8, Natividad R. Stover8, Rebecca McMurray8, Mark F. Lew9, Connie Kawai9, David Coffey10, Pauline LeBlanc10, Julie H. Carter11, Matthew Brodsky11, Pamela Andrews11, Andrew Siderowf12, Sue Reichwein12, Lisa M. Shulman13, William J. Weiner13, Katharine Pabst13, Jeana Jaglin4, Robert A. Hauser14, Theresa McClain14, Holly Delgado14, Oksana Suchowersky15, Lorelei Derwent15, Jayaraman Rao16, Maureen Cook16, Michael J. Aminoff17, Chad W. Christine17, Jessie Roth17, Maureen A. Leehey18, Jacci Bainbridge18, G. Webster Ross, Stephanie Terashita, Carlos Singer19, Marian A. Perez19, Anita Blenke19, Brad A. Racette20, Patricia Deppen20, Rodger J. Elble21, Charlene Young21, Tracy Stewart, Kapil D. Sethi22, Buff Dill22, John W. Taylor23, Peggy Roberge23, Richard B. Dewey24, Brigid Hayward24, Joseph Jankovic25, Christine Hunter25, Frederick Wooten5, Margaret F. Keller5, Danna Jennings, Tammie Kelsey, W.R. Wayne Martin26, Germaine McInnes26, Joanne Wojcieszek27, Joann Belden27, Roger L. Albin28, Kristine Wernette28, Joseph M. Savitt29, Becky Dunlop29, Rajesh Pahwa30, Kelly E. Lyons30, Amy Parsons30, John Y. Fang31, Dorothy Shearon31, Andrew Feigin32, Margaret Marie Cox32, Charles H. Adler33, Marlene Lind33, Burton L. Scott34, Joanne Field34, Martha Nance, Susan Peterson, Richard S. Burns35, Lynn Marlor35, I. Van Bodis-Wollner36, Elizabeth Hayes36, Jay S. Schneider37, Stephanie Sendek37, Stephen Gollomp37, Gwyn Vernon37, Peter A LeWitt38, Maryan DeAngelis38, David Simon39, Linda Paul39, Jay M. Gorell40, Shana Krstevska40, Marilyn Flewellen40, Sharon McCarthy40, Ryan J. Uitti33, Margaret F. Turk33, James H. Bower33, Susan Torgrimson33, Marwan N. Sabbagh, Zoran Obradov, Jorge L. Juncos41, Mary Louise Musante Weeks41, Hubert H. Fernandez42, Gordon H. Brown42, Jordan J. Elm3, Paulo Guimaraes3, Peng Huang3, Yuko Y. Palesch3, Cornelia Kamp1, Aileen Shinaman1, Debbie Fraser1, Alicia Brocht1, Susan Bennett1, Chris Weaver1, Debbie Baker1, Beverly Olsen1, Christopher G. Goetz4, Janis M. Miyasaki43, Susan C. Fagan44, Patrick D. Mauldin3 
TL;DR: Coenzyme Q10 and GPI-1485 may warrant further study in Parkinson disease, although the data are inconsistent, and additional factors should be considered in the selection of agents for Phase III studies.
Abstract: Objective: To determine if future studies of coenzyme Q10 and GPI-1485 in Parkinson disease (PD) may be warranted. Methods: We conducted a randomized, double-blind, calibrated futility clinical trial of coenzyme Q10 and GPI-1485 in early untreated PD using placebo data from the DATATOP study to establish the futility threshold. Results: The primary outcome measure (change in total Unified Parkinson's Disease Rating Scale scores over 1 year) did not meet the prespecified criteria for futility for either agent. Secondary analyses using calibration controls and other more recent placebo data question the appropriateness of the predetermined definition of futility, and suggest that a more restrictive threshold may be needed. Conclusions: Coenzyme Q10 and GPI-1485 may warrant further study in Parkinson disease, although the data are inconsistent. Additional factors (cost, availability of other agents, more recent data on placebo outcomes, other ongoing trials) should also be considered in the selection of agents for Phase III studies. NEUROLOGY 2007;68:20-28

209 citations


Cited by
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TL;DR: Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures, and measures should be taken to reduce cadmiam exposure in the general population in order to minimize the risk of adverse health results.
Abstract: The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic. These metals have been extensively studied and their effects on human health regularly reviewed by international bodies such as the WHO. Heavy metals have been used by humans for thousands of years. Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. Cadmium compounds are currently mainly used in re-chargeable nickel-cadmium batteries. Cadmium emissions have increased dramatically during the 20th century, one reason being that cadmium-containing products are rarely re-cycled, but often dumped together with household waste. Cigarette smoking is a major source of cadmium exposure. In non-smokers, food is the most important source of cadmium exposure. Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects. The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure, and dental amalgam. The general population does not face a significant health risk from methyl mercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from polluted fresh waters should especially be avoided. There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases. However, there are no studies so far that have been able to show any associations between amalgam fillings and ill health. The general population is exposed to lead from air and food in roughly equal proportions. During the last century, lead emissions to ambient air have caused considerable pollution, mainly due to lead emissions from petrol. Children are particularly susceptible to lead exposure due to high gastrointestinal uptake and the permeable blood-brain barrier. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically decreased over the last decades, thereby reducing environmental exposure, phasing out any remaining uses of lead additives in motor fuels should be encouraged. The use of lead-based paints should be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food. Exposure to arsenic is mainly via intake of food and drinking water, food being the most important source in most populations. Long-term exposure to arsenic in drinking-water is mainly related to increased risks of skin cancer, but also some other cancers, as well as other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure-response relationships and high risks have been observed.

5,015 citations

Journal ArticleDOI
TL;DR: The Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity, and two levels of certainty are delineated: clinically established PD and probable PD.
Abstract: This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.

3,421 citations

Journal ArticleDOI
TL;DR: Environmental lead exposure in children who have maximal blood lead levels < 7.5 μg/dL is associated with intellectual deficits, and an inverse relationship between blood lead concentration and IQ score is found.
Abstract: Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 µg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 µg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5‐10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 µg/dL and declined to 9.4 µg/dL by 5‐7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 µg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 µg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a loglinear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2‐9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 µg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 µg/dL, 10 to 20 µg/dL, and 20 to 30 µg/dL were 3.9 (95% CI, 2.4‐5.3), 1.9 (95% CI, 1.2‐2.6), and 1.1 (95% CI, 0.7‐1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 µg/dL was significantly greater than that observed for those with a maximal blood lead level ≥ 7.5 µg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 µg/dL is asso

1,945 citations

Journal ArticleDOI
TL;DR: Evidence has accumulated pointing to socioeconomic factors such as income, wealth, and education as the fundamental causes of a wide range of health outcomes, and plausible pathways and biological mechanisms that may explain their effects are reviewed.
Abstract: During the past two decades, the public health community’s attention has been drawn increasingly to the social determinants of health (SDH)—the factors apart from medical care that can be influenced by social policies and shape health in powerful ways. We use “medical care” rather than “health care” to refer to clinical services, to avoid potential confusion between “health” and “health care.” The World Health Organization’s Commission on the Social Determinants of Health has defined SDH as “the conditions in which people are born, grow, live, work and age” and “the fundamental drivers of these conditions.” The term “social determinants” often evokes factors such as health-related features of neighborhoods (e.g., walkability, recreational areas, and accessibility of healthful foods), which can influence health-related behaviors. Evidence has accumulated, however, pointing to socioeconomic factors such as income, wealth, and education as the fundamental causes of a wide range of health outcomes. This article broadly reviews some of the knowledge accumulated to date that highlights the importance of social—and particularly socioeconomic— factors in shaping health, and plausible pathways and biological mechanisms that may explain their effects. We also discuss challenges to advancing this knowledge and how they might be overcome.

1,856 citations