Parkinson Disease: Goldman S

Vander Borght T, Laloux P, Maes A, Salmon E, Goethals I, Goldman S, Anonymous00187. · Nuclear Medicine Division, Mont-Godinne Medical Center, Université Catholique de Louvain, B-5530 Yvoir, Belgium. · Acta Neurol Belg. · Pubmed #11851026 No free full text.

Abstract: The purpose of these guidelines is to assist nuclear medicine practitioners in recommending, performing, interpreting, and reporting the results of brain perfusion SPECT studies using Tc-99m radiopharmaceuticals and brain metabolism PET studies using F-18 fluorodeoxyglucose (FDG). These guidelines have been adapted and extended from those produced by the Society of Nuclear Medicine (Juni et al., 1998) and the European Association of Nuclear Medicine by a Belgian group of experts in the field trained in neurology and/or nuclear medicine. Some indications are not universally approved (e.g. brain death), but largely supported by the literature. They have been included in these guidelines in order to provide recommendations and a standardised protocol.

Kamel F, Tanner C, Umbach D, Hoppin J, Alavanja M, Blair A, Comyns K, Goldman S, Korell M, Langston J, Ross G, Sandler D. · National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. · Am J Epidemiol. · Pubmed #17116648 links to  free full text

Abstract: Previous studies based on limited exposure assessment have suggested that Parkinson's disease (PD) is associated with pesticide exposure. The authors used data obtained from licensed private pesticide applicators and spouses participating in the Agricultural Health Study to evaluate the relation of self-reported PD to pesticide exposure. Cohort members, who were enrolled in 1993-1997, provided detailed information on lifetime pesticide use. At follow-up in 1999-2003, 68% of the cohort was interviewed. Cases were defined as participants who reported physician-diagnosed PD at enrollment (prevalent cases, n = 83) or follow-up (incident cases, n = 78). Cases were compared with cohort members who did not report PD (n = 79,557 at enrollment and n = 55,931 at follow-up). Incident PD was associated with cumulative days of pesticide use at enrollment (for highest quartile vs. lowest, odds ratio (OR) = 2.3, 95% confidence interval: 1.2, 4.5; p-trend = 0.009), with personally applying pesticides more than half the time (OR = 1.9, 95% confidence interval: 0.7, 4.7), and with some specific pesticides (ORs > or = 1.4). Prevalent PD was not associated with overall pesticide use. This study suggests that exposure to certain pesticides may increase PD risk. Findings for specific chemicals may provide fruitful leads for further investigation.

Goldman S. · Division of Cell and Gene Therapy, Department of Neurology, 601 Elmwood Ave., Box 645, University of Rochester Medical Center, Rochester, New York 14642, USA. · Nat Biotechnol. · Pubmed #16003375 No free full text.

Abstract: Multipotent neural stem cells, capable of giving rise to both neurons and glia, line the cerebral ventricles of all adult animals, including humans. In addition, distinct populations of nominally glial progenitor cells, which also have the capacity to generate several cell types, are dispersed throughout the subcortical white matter and cortex. A number of approaches have evolved for using neural progenitor cells in cell therapy. Four strategies are especially attractive for clinical translation: first, transplantation of oligodendrocyte progenitor cells as a means of treating the disorders of myelin; second, transplantation of phenotypically restricted neuronal progenitor cells to treat diseases of discrete loss of a single neuronal phenotype, such as Parkinson disease; third, implantation of mixed progenitor pools to treat diseases characterized by the loss of several discrete phenotypes, such as spinal cord injury; and fourth, mobilization of endogenous neural progenitor cells to restore neurons lost as a result of neurodegenerative diseases, in particular Huntington disease. Together, these may present the most compelling strategies and near-term disease targets for cell-based neurological therapy.

Marras C, Goldman S, Smith A, Barney P, Aston D, Comyns K, Korell M, Langston JW, Ross GW, Tanner CM. · The Parkinson's Institute, Sunnyvale, California, USA. · Mov Disord. · Pubmed #15719425 No free full text.

Abstract: Olfactory dysfunction has been proposed to be a sign that may precede the motor features of Parkinson's disease (PD). To determine whether smell identification deficits predict subsequent PD, we studied smell identification ability using the University of Pennsylvania Smell Identification Test (UPSIT) in 62 members of male twin pairs discordant for PD at baseline. Smell identification ability was reduced at baseline in the twins with PD compared to their unaffected brothers (23 vs. 31 of 40; P = 0.001). UPSIT scores were not reduced in the twins without PD when compared to age- and gender-specific normal values. After a mean interval of 7.3 years, 28 unaffected twins were still alive and 19 agreed to a second evaluation. Two had newly developed PD. Neither twin had impaired smell identification at baseline. The average decline in UPSIT percentile scores in these 2 twins was greater than in the 17 twins who did not develop PD (-68% vs. -24%; P = 0.01). In subjects who did not meet Core Assessment Program for Intracerebral Transplantations diagnostic criteria for PD at baseline, the presence of cardinal signs of parkinsonism was not associated with lower baseline UPSIT scores nor with a subsequent decline. Smell identification ability may not be a sensitive indicator of future PD 7 or more years before the development of motor signs, even in a theoretically at-risk population.

Dethy S, Laute MA, Damhaut P, Goldman S. · Service de Neurologie, ULB-Hôpital Erasme, Brussels, Belgium. · J Neural Transm. · Pubmed #10226935 No free full text.

Abstract: We used intrastriatal microdialysis to study the effect of pergolide, a D1/D2 dopamine (DA) receptor agonist on biotransformation of exogenous L-DOPA in hemi-Parkinsonian rats. DA and metabolites were assayed by microbore liquid chromatography. Pergolide (50 micrograms/kg, i.p.) caused a 67% and 87% decrease in striatal EC levels of DA in intact and denervated striatum respectively. In intact striatum but not in denervated striatum, pergolide decreased EC levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) (53% and 42% decrease, respectively). L-DOPA (100 mg/kg, i.p.) produced significant increase in EC levels of DA, DOPAC and HVA in intact and denervated striatum with and without local perfusion of 10(-4) M pergolide. In denervated striatum, L-DOPA-induced DA increase was significantly higher in rats with pergolide. Our results suggest that, in an animal model of Parkinson's disease, pergolide in association with L-DOPA favors the restoration of striatal EC DA levels.

Bronstein J, Carvey P, Chen H, Cory-Slechta D, DiMonte D, Duda J, English P, Goldman S, Grate S, Hansen J, Hoppin J, Jewell S, Kamel F, Koroshetz W, Langston JW, Logroscino G, Nelson L, Ravina B, Rocca W, Ross GW, Schettler T, Schwarzschild M, Scott B, Seegal R, Singleton A, Steenland K, Tanner CM, Van Den Eeden S, Weisskopf M. · UCLA School of Medicine, Los Angeles, California, USA. · Environ Health Perspect. · Pubmed #19165397 links to  free full text

Abstract: BACKGROUND: Parkinson's disease (PD) is the second most common neurodegenerative disorder. People with PD, their families, scientists, health care providers, and the general public are increasingly interested in identifying environmental contributors to PD risk. METHODS: In June 2007, a multidisciplinary group of experts gathered in Sunnyvale, California, USA, to assess what is known about the contribution of environmental factors to PD. RESULTS: We describe the conclusions around which they came to consensus with respect to environmental contributors to PD risk. We conclude with a brief summary of research needs. CONCLUSIONS: PD is a complex disorder, and multiple different pathogenic pathways and mechanisms can ultimately lead to PD. Within the individual there are many determinants of PD risk, and within populations, the causes of PD are heterogeneous. Although rare recognized genetic mutations are sufficient to cause PD, these account for < 10% of PD in the U.S. population, and incomplete penetrance suggests that environmental factors may be involved. Indeed, interplay among environmental factors and genetic makeup likely influences the risk of developing PD. There is a need for further understanding of how risk factors interact, and studying PD is likely to increase understanding of other neurodegenerative disorders.