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266 results on '"Hurtig, H."'

4. Hippocampal subfield pathologic burden in Lewy body diseases vs. Alzheimer’s disease

Author

Coughlin, D. G., primary, Ittyerah, R., additional, Peterson, C., additional, Phillips, J. S., additional, Miller, S., additional, Rascovsky, K., additional, Weintraub, D., additional, Siderowf, A. D., additional, Duda, J. E., additional, Hurtig, H. I., additional, Wolk, D. A., additional, McMillan, C. T., additional, Yushkevich, P. A., additional, Grossman, M., additional, Lee, E. B., additional, Trojanowski, J. Q., additional, and Irwin, D. J., additional

Published
2020
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10. A Double-Blind, Delayed-Start Trial of Rasagiline in Parkinson's Disease

Author

Olanow, Cw, Rascol, O, Hauser, R, Feigin, Pd, Jankovic, J, Lang, A, Langston, W, Melamed, E, Poewe, W, Stocchi, F, Tolosa, E, ADAGIO STUDY INVESTIGATORS, Collaborators, Bueri, J, Garretto, N, Gershanik, O, Giannaula, R, Micheli, F, Wolf, E, Guttman, M, Hobson, D, Jog, M, King, D, Mendis, T, Miyasaki, J, Panisset, M, Pourcher, E, Rajput, A, Ranawaya, R, Tsui, J, Cesaro, P, Damier, P, Destee, A, Durif, F, Slaoui, T, Tison, F, Viallet, F, Deuschl, G, Gasser, T, Ludolph, A, Oehlwein, C, Przuntek, H, Reifschneider, G, Schnitzler, A, Trenkwalder, C, Bokor, M, Katona, A, Lajtos, J, Nikl, J, Takats, A, Valikovics, A, Badarny, S, Djaldetti, R, Giladi, N, Hassin, S, Rabey, Jm, Reches, A, Schwartz, M, Wirguin, I, Albanese, A, Bentivoglio, A, Bonuccelli, U, Calzetti, S, Comi, G, Curatola, L, Ferrarese, C, Lamberti, P, Marconi, R, Martignoni, E, Meco, Giuseppe, Ruggieri, Stefano, Bomhof, Ma, Hovestadt, A, Krul, Jm, Leenders, Kl, Cunha, L, Ferreira, J, Bajenaru, Oa, Carciumaru, N, Bulboaca, Ac, Pascu, I, Simu, M, Calopa, M, FERNÁNDEZ GARCÍA JM, Kulisevsky, J, Linazasoro, C, Miquel, F, Posada, Ij, Martí, Mj, Burn, D, Macmahon, D, Barker, R, Allen, N, Barbour, P, Bertoni, J, Bharucha, K, Bose, S, Drasby, E, Elble, R, Elmer, L, Evans, B, Factor, S, Fernandez, H, Friedman, J, Hull, K, Golbe, L, Goudreau, J, Guttuso, T, Hassan, M, Hermanowicz, N, Houser, M, Hurtig, H, Isaacson, S, Jennings, D, Kompoliti, A, Morgan, J, Murphy, J, Nausieda, P, Pahwa, R, Parashos, S, O'Suilleabhain, P, Racette, B, Reich, S, Roberts, J, Rothstein, T, Sahay, A, SAINT HILAIRE, M, Schiess, M, Scott, B, Shahed, J, Simuni, T, Singer, C, Smith, R, Struck, L, Sutton, J, Swope, D, Tagliati, M, Tetrud, J, Togasaki, D, Watts, R., Olanow, C, Rascol, O, Hauser, R, Feigin, P, Jankovic, J, Lang, A, Langston, W, Melamed, E, Poewe, W, Stocchi, F, Tolosa, E, ADAGIO Study, I, Bueri, J, Garretto, N, Gershanik, O, Giannaula, R, Micheli, F, Wolf, E, Guttman, M, Hobson, D, Jog, M, King, D, Mendis, T, Miyasaki, J, Panisset, M, Pourcher, E, Rajput, A, Ranawaya, R, Tsui, J, Cesaro, P, Damier, P, Destee, A, Durif, F, Slaoui, T, Tison, F, Viallet, F, Deuschl, G, Gasser, T, Ludolph, A, Oehlwein, C, Przuntek, H, Reifschneider, G, Schnitzler, A, Trenkwalder, C, Bokor, M, Katona, A, Lajtos, J, Nikl, J, Takats, A, Valikovics, A, Badarny, S, Djaldetti, R, Giladi, N, Hassin, S, Rabey, J, Reches, A, Schwartz, M, Wirguin, I, Albanese, A, Bentivoglio, A, Bonuccelli, U, Calzetti, S, Comi, G, Curatola, L, Ferrarese, C, Lamberti, P, Marconi, R, Martignoni, E, Meco, G, Ruggieri, S, Bomhof, M, Hovestadt, A, Krul, J, Leenders, K, Cunha, L, Ferreira, J, Bajenaru, O, Carciumaru, N, Bulboaca, A, Pascu, I, Simu, M, Calopa, M, Fernández García, J, Kulisevsky, J, Linazasoro, C, Miquel, F, Posada, I, Martí, M, Burn, D, Macmahon, D, Barker, R, Allen, N, Barbour, P, Bertoni, J, Bharucha, K, Bose, S, Drasby, E, Elble, R, Elmer, L, Evans, B, Factor, S, Fernandez, H, Friedman, J, Hull, K, Golbe, L, Goudreau, J, Guttuso, T, Hassan, M, Hermanowicz, N, Houser, M, Hurtig, H, Isaacson, S, Jennings, D, Kompoliti, A, Morgan, J, Murphy, J, Nausieda, P, Pahwa, R, Parashos, S, O'Suilleabhain, P, Racette, B, Reich, S, Roberts, J, Rothstein, T, Sahay, A, Saint Hilaire, M, Schiess, M, Scott, B, Shahed, J, Simuni, T, Singer, C, Smith, R, Struck, L, Sutton, J, Swope, D, Tagliati, M, Tetrud, J, Togasaki, D, and Watts, R

Subjects
Adult, Male, medicine.medical_specialty, Monoamine Oxidase Inhibitors, Parkinson's disease, Neuroprotective Agent, Severe disease, Placebo, Severity of Illness Index, Placebo group, Drug Administration Schedule, Central nervous system disease, Double blind, chemistry.chemical_compound, Double-Blind Method, Severity of illness, Humans, Rasagiline, Medicine, Monoamine Oxidase Inhibitor, Aged, Dose-Response Relationship, Drug, business.industry, Indan, Parkinson Disease, General Medicine, Middle Aged, medicine.disease, Surgery, Neuroprotective Agents, chemistry, Research Design, Anesthesia, Indans, Female, business, Human
Abstract

BACKGROUND: A therapy that slows disease progression is the major unmet need in Parkinson's disease. METHODS: In this double-blind trial, we examined the possibility that rasagiline has disease-modifying effects in Parkinson's disease. A total of 1176 subjects with untreated Parkinson's disease were randomly assigned to receive rasagiline (at a dose of either 1 mg or 2 mg per day) for 72 weeks (the early-start group) or placebo for 36 weeks followed by rasagiline (at a dose of either 1 mg or 2 mg per day) for 36 weeks (the delayed-start group). To determine a positive result with either dose, the early-start treatment group had to meet each of three hierarchical end points of the primary analysis based on the Unified Parkinson's Disease Rating Scale (UPDRS, a 176-point scale, with higher numbers indicating more severe disease): superiority to placebo in the rate of change in the UPDRS score between weeks 12 and 36, superiority to delayed-start treatment in the change in the score between baseline and week 72, and noninferiority to delayed-start treatment in the rate of change in the score between weeks 48 and 72. RESULTS: Early-start treatment with rasagiline at a dose of 1 mg per day met all end points in the primary analysis: a smaller mean (+/-SE) increase (rate of worsening) in the UPDRS score between weeks 12 and 36 (0.09+/-0.02 points per week in the early-start group vs. 0.14+/-0.01 points per week in the placebo group, P=0.01), less worsening in the score between baseline and week 72 (2.82+/-0.53 points in the early-start group vs. 4.52+/-0.56 points in the delayed-start group, P=0.02), and noninferiority between the two groups with respect to the rate of change in the UPDRS score between weeks 48 and 72 (0.085+/-0.02 points per week in the early-start group vs. 0.085+/-0.02 points per week in the delayed-start group, P

Published
2009

18. Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type

Author

Brettschneider, J., primary, Irwin, D. J., additional, Boluda, S., additional, Byrne, M. D., additional, Fang, L., additional, Lee, E. B., additional, Robinson, J. L., additional, Suh, E., additional, Van Deerlin, V. M., additional, Toledo, J. B., additional, Grossman, M., additional, Hurtig, H., additional, Dengler, R., additional, Petri, S., additional, Lee, V. M.-Y., additional, and Trojanowski, J. Q., additional

Published
2016
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19. Clinical and Biochemical Differences in Parkinson’s Patients With and Without GBA Mutations

Author

Chahine, LM, Qiang, JK, Ashbridge, E, Minger, J, Yearout, D, Horn, S, Colcher, A, Hurtig, H, Lee, VM, Van Deerlin, VM, Leverenz, JB, Siderowf, A, Trojanowski, JQ, Zabetian, CP, and Chen-Plotkin, A

Subjects
Male, Genotype, beta-Glucosidase, Age Factors, Parkinson Disease, Blood Proteins, Middle Aged, Article, Cohort Studies, Phenotype, Case-Control Studies, Mutation, Humans, Female, Genetic Predisposition to Disease, Age of Onset, Aged
Abstract

Biochemical abnormalities present in GBA (mut/wt) carriers may offer new pathogenetic insights to and potential therapeutic targets in Parkinson disease (PD).To determine whether patients having PD with vs without GBA mutations differ in clinical phenotype or plasma protein expression.Case-control study of patients having PD with vs without GBA mutations. Clinical characteristics were compared between groups, and biochemical profiling of 40 plasma proteins was performed to identify proteins that differed in expression between groups.The discovery cohort included 20 patients having PD with GBA mutations. Clinical characteristics of GBA-associated PD cases were compared with those of 242 patients having PD in whom GBA mutations were excluded by full gene sequencing.Biochemical profiling was available for all 20 GBA-associated PD cases, as well as a subset (87 of 242) of the GBA-negative PD cases. The replication cohort included 19 patients having PD with GBA mutations and 41 patients having PD without GBA mutations.Compared with patients having PD without GBA mutations, patients having PD with GBA mutations were younger at disease onset (P = .04) and were more likely to demonstrate cognitive dysfunction (P = .001). In a multiple regression model that included age, sex, and assay batch as covariates, GBA mutation status was significantly associated with plasma levels of interleukin 8 (P = .001), monocyte chemotactic protein 1 (P = .008), and macrophage inflammatory protein 1α (P = .005). The association between interleukin 8 and GBA mutation status was replicated (P = .03) in a separate cohort of patients having PD with vs without GBA mutations.Patients having PD with GBA mutations have earlier age at disease onset and are more likely to demonstrate cognitive dysfunction. Monocyte-associated inflammatory mediators may be elevated in patients having PD with GBA mutations.

Published
2013

20. Treatment of organic bipolar mood disorders in Parkinson's disease

Author

David Glosser, Zwil As, Hurtig H, Kim E, Stern M, and McAllister Tw

Subjects
Male, Levodopa, medicine.medical_specialty, Bipolar Disorder, Parkinson's disease, Lithium (medication), Psychoses, Substance-Induced, chemistry.chemical_compound, Lithium Carbonate, Recurrence, mental disorders, medicine, Humans, Bipolar disorder, Psychiatry, Clozapine, business.industry, Lithium carbonate, Parkinson Disease, Middle Aged, medicine.disease, Psychiatry and Mental health, Mood disorders, chemistry, Drug Therapy, Combination, Female, Neurology (clinical), medicine.symptom, business, Mania, medicine.drug
Abstract

Two patients with long-standing idiopathic Parkinson's disease (PD), without individual or family histories of affective disorders, developed bipolar mood disorders. Both were treated with lithium and clozapine, and one responded favorably. These may be the first reported cases in which mania was treated with clozapine in PD patients.

Published
1994

22. PARK10 is a major locus for sporadic neuropathologically confirmed Parkinson disease

Author

Beecham, G. W., primary, Dickson, D. W., additional, Scott, W. K., additional, Martin, E. R., additional, Schellenberg, G., additional, Nuytemans, K., additional, Larson, E. B., additional, Buxbaum, J. D., additional, Trojanowski, J. Q., additional, Van Deerlin, V. M., additional, Hurtig, H. I., additional, Mash, D. C., additional, Beach, T. G., additional, Troncoso, J. C., additional, Pletnikova, O., additional, Frosch, M. P., additional, Ghetti, B., additional, Foroud, T. M., additional, Honig, L. S., additional, Marder, K., additional, Vonsattel, J. P., additional, Goldman, S. M., additional, Vinters, H. V., additional, Ross, O. A., additional, Wszolek, Z. K., additional, Wang, L., additional, Dykxhoorn, D. M., additional, Pericak-Vance, M. A., additional, Montine, T. J., additional, Leverenz, J. B., additional, Dawson, T. M., additional, and Vance, J. M., additional

Published
2015
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23. Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type.

Author

Brettschneider, J., Irwin, D. J., Boluda, S., Byrne, M. D., Fang, L., Lee, E. B., Robinson, J. L., Suh, E., Van Deerlin, V. M., Toledo, J. B., Grossman, M., Hurtig, H., Dengler, R., Petri, S., Lee, V. M.‐Y., and Trojanowski, J. Q.

Subjects
ALPHA-synuclein, MULTIPLE system atrophy, CEREBELLUM degeneration, NEUROGLIA, DISEASE progression
Abstract

Aims The aim of this study was to identify early foci of α-synuclein (α-syn pathology) accumulation, subsequent progression and neurodegeneration in multiple system atrophy of the cerebellar type (MSA-C). Methods We analysed 70-μm-thick sections of 10 cases with MSA-C and 24 normal controls. Results MSA-C cases with the lowest burden of pathology showed α-syn glial cytoplasmic inclusions (GCIs) in the cerebellum as well as in medullary and pontine cerebellar projections. Cerebellar pathology was highly selective and severely involved subcortical white matter, whereas deep white matter and granular layer were only mildly affected and the molecular layer was spared. Loss of Purkinje cells increased with disease duration and was associated with neuronal and axonal abnormalities. Neocortex, basal ganglia and spinal cord became consecutively involved with the increasing burden of α-syn pathology, followed by hippocampus, amygdala, and, finally, the visual cortex. GCIs were associated with myelinated axons, and the severity of GCIs correlated with demyelination. Conclusions Our findings indicate that cerebellar subcortical white matter and cerebellar brainstem projections are likely the earliest foci of α-syn pathology in MSA-C, followed by involvement of more widespread regions of the central nervous system and neurodegeneration with disease progression. [ABSTRACT FROM AUTHOR]

Published
2017
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25. A double-blind, delayed-start trial of rasagiline in Parkinson's disease

Author

Olanow, C, Rascol, O, Hauser, R, Feigin, P, Jankovic, J, Lang, A, Langston, W, Melamed, E, Poewe, W, Stocchi, F, Tolosa, E, ADAGIO Study, I, Bueri, J, Garretto, N, Gershanik, O, Giannaula, R, Micheli, F, Wolf, E, Guttman, M, Hobson, D, Jog, M, King, D, Mendis, T, Miyasaki, J, Panisset, M, Pourcher, E, Rajput, A, Ranawaya, R, Tsui, J, Cesaro, P, Damier, P, Destee, A, Durif, F, Slaoui, T, Tison, F, Viallet, F, Deuschl, G, Gasser, T, Ludolph, A, Oehlwein, C, Przuntek, H, Reifschneider, G, Schnitzler, A, Trenkwalder, C, Bokor, M, Katona, A, Lajtos, J, Nikl, J, Takats, A, Valikovics, A, Badarny, S, Djaldetti, R, Giladi, N, Hassin, S, Rabey, J, Reches, A, Schwartz, M, Wirguin, I, Albanese, A, Bentivoglio, A, Bonuccelli, U, Calzetti, S, Comi, G, Curatola, L, Ferrarese, C, Lamberti, P, Marconi, R, Martignoni, E, Meco, G, Ruggieri, S, Bomhof, M, Hovestadt, A, Krul, J, Leenders, K, Cunha, L, Ferreira, J, Bajenaru, O, Carciumaru, N, Bulboaca, A, Pascu, I, Simu, M, Calopa, M, Fernández García, J, Kulisevsky, J, Linazasoro, C, Miquel, F, Posada, I, Martí, M, Burn, D, Macmahon, D, Barker, R, Allen, N, Barbour, P, Bertoni, J, Bharucha, K, Bose, S, Drasby, E, Elble, R, Elmer, L, Evans, B, Factor, S, Fernandez, H, Friedman, J, Hull, K, Golbe, L, Goudreau, J, Guttuso, T, Hassan, M, Hermanowicz, N, Houser, M, Hurtig, H, Isaacson, S, Jennings, D, Kompoliti, A, Morgan, J, Murphy, J, Nausieda, P, Pahwa, R, Parashos, S, O'Suilleabhain, P, Racette, B, Reich, S, Roberts, J, Rothstein, T, Sahay, A, Saint Hilaire, M, Schiess, M, Scott, B, Shahed, J, Simuni, T, Singer, C, Smith, R, Struck, L, Sutton, J, Swope, D, Tagliati, M, Tetrud, J, Togasaki, D, Watts, R, Olanow, CW, Feigin, PD, ADAGIO Study Investigators, Rabey, JM, FERRARESE, CARLO, Bomhof, MA, Krul, JM, Leenders, KL, Bajenaru, OA, Bulboaca, AC, Fernández García, JM, Posada, IJ, Martí, MJ, MacMahon, D, Watts, R., Olanow, C, Rascol, O, Hauser, R, Feigin, P, Jankovic, J, Lang, A, Langston, W, Melamed, E, Poewe, W, Stocchi, F, Tolosa, E, ADAGIO Study, I, Bueri, J, Garretto, N, Gershanik, O, Giannaula, R, Micheli, F, Wolf, E, Guttman, M, Hobson, D, Jog, M, King, D, Mendis, T, Miyasaki, J, Panisset, M, Pourcher, E, Rajput, A, Ranawaya, R, Tsui, J, Cesaro, P, Damier, P, Destee, A, Durif, F, Slaoui, T, Tison, F, Viallet, F, Deuschl, G, Gasser, T, Ludolph, A, Oehlwein, C, Przuntek, H, Reifschneider, G, Schnitzler, A, Trenkwalder, C, Bokor, M, Katona, A, Lajtos, J, Nikl, J, Takats, A, Valikovics, A, Badarny, S, Djaldetti, R, Giladi, N, Hassin, S, Rabey, J, Reches, A, Schwartz, M, Wirguin, I, Albanese, A, Bentivoglio, A, Bonuccelli, U, Calzetti, S, Comi, G, Curatola, L, Ferrarese, C, Lamberti, P, Marconi, R, Martignoni, E, Meco, G, Ruggieri, S, Bomhof, M, Hovestadt, A, Krul, J, Leenders, K, Cunha, L, Ferreira, J, Bajenaru, O, Carciumaru, N, Bulboaca, A, Pascu, I, Simu, M, Calopa, M, Fernández García, J, Kulisevsky, J, Linazasoro, C, Miquel, F, Posada, I, Martí, M, Burn, D, Macmahon, D, Barker, R, Allen, N, Barbour, P, Bertoni, J, Bharucha, K, Bose, S, Drasby, E, Elble, R, Elmer, L, Evans, B, Factor, S, Fernandez, H, Friedman, J, Hull, K, Golbe, L, Goudreau, J, Guttuso, T, Hassan, M, Hermanowicz, N, Houser, M, Hurtig, H, Isaacson, S, Jennings, D, Kompoliti, A, Morgan, J, Murphy, J, Nausieda, P, Pahwa, R, Parashos, S, O'Suilleabhain, P, Racette, B, Reich, S, Roberts, J, Rothstein, T, Sahay, A, Saint Hilaire, M, Schiess, M, Scott, B, Shahed, J, Simuni, T, Singer, C, Smith, R, Struck, L, Sutton, J, Swope, D, Tagliati, M, Tetrud, J, Togasaki, D, Watts, R, Olanow, CW, Feigin, PD, ADAGIO Study Investigators, Rabey, JM, FERRARESE, CARLO, Bomhof, MA, Krul, JM, Leenders, KL, Bajenaru, OA, Bulboaca, AC, Fernández García, JM, Posada, IJ, Martí, MJ, MacMahon, D, and Watts, R.

Abstract

BACKGROUND: A therapy that slows disease progression is the major unmet need in Parkinson's disease. METHODS: In this double-blind trial, we examined the possibility that rasagiline has disease-modifying effects in Parkinson's disease. A total of 1176 subjects with untreated Parkinson's disease were randomly assigned to receive rasagiline (at a dose of either 1 mg or 2 mg per day) for 72 weeks (the early-start group) or placebo for 36 weeks followed by rasagiline (at a dose of either 1 mg or 2 mg per day) for 36 weeks (the delayed-start group). To determine a positive result with either dose, the early-start treatment group had to meet each of three hierarchical end points of the primary analysis based on the Unified Parkinson's Disease Rating Scale (UPDRS, a 176-point scale, with higher numbers indicating more severe disease): superiority to placebo in the rate of change in the UPDRS score between weeks 12 and 36, superiority to delayed-start treatment in the change in the score between baseline and week 72, and noninferiority to delayed-start treatment in the rate of change in the score between weeks 48 and 72. RESULTS: Early-start treatment with rasagiline at a dose of 1 mg per day met all end points in the primary analysis: a smaller mean (+/-SE) increase (rate of worsening) in the UPDRS score between weeks 12 and 36 (0.09+/-0.02 points per week in the early-start group vs. 0.14+/-0.01 points per week in the placebo group, P=0.01), less worsening in the score between baseline and week 72 (2.82+/-0.53 points in the early-start group vs. 4.52+/-0.56 points in the delayed-start group, P=0.02), and noninferiority between the two groups with respect to the rate of change in the UPDRS score between weeks 48 and 72 (0.085+/-0.02 points per week in the early-start group vs. 0.085+/-0.02 points per week in the delayed-start group, P<0.001). All three end points were not met with rasagiline at a dose of 2 mg per day, since the change in the UPDRS score between baseline

Published
2009

28. Clinical and Biochemical Differences between Parkinson's Disease Patients With and Without Mutations in the Glucocerebrosidase Gene (P06.072)

Author

Chahine, L., primary, Ashbridge, E., additional, Minger, J., additional, Yearout, D., additional, Qiang, J., additional, Siderowf, A., additional, Hurtig, H., additional, Zabetian, C., additional, Lee, V., additional, Van Deerlin, V., additional, Trojanowski, J., additional, and Chen-Plotkin, A., additional

Published
2012
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29. Phosphorylated ? -Synuclein in Parkinson's Disease

Author

Wang, Y., Shi, M., Chung, K. A., Zabetian, C. P., Leverenz, J. B., Berg, D., Srulijes, K., Trojanowski, J. Q., Lee, V. M.- Y., Siderowf, A. D., Hurtig, H., Litvan, I., Schiess, M. C., Peskind, E. R., Masuda, M., Hasegawa, M., Lin, X., Pan, C., Galasko, D., Goldstein, D. S., Jensen, P. H., Yang, H., Cain, K. C., and Zhang, J.

Published
2012
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30. Novel CSF biomarkers for frontotemporal lobar degenerations

Author

Hu, W. T., primary, Chen-Plotkin, A., additional, Grossman, M., additional, Arnold, S. E., additional, Clark, C. M., additional, Shaw, L. M., additional, McCluskey, L., additional, Elman, L., additional, Hurtig, H. I., additional, Siderowf, A., additional, Lee, V. M.- Y., additional, Soares, H., additional, and Trojanowski, J. Q., additional

Published
2010
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35. Das Leben von F. H. Lewy

Author

Rodrigues e Silva, A.M, primary, Holdorff, B, additional, Kielhorn, F.W, additional, Hurtig, H, additional, and Dodel, R, additional

Published
2008
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36. Longitudinal decline in autopsy-defined frontotemporal lobar degeneration

Author

Grossman, M., primary, Xie, S. X., additional, Libon, D. J., additional, Wang, X., additional, Massimo, L., additional, Moore, P., additional, Vesely, L., additional, Berkowitz, R., additional, Chatterjee, A., additional, Coslett, H. B., additional, Hurtig, H. I., additional, Forman, M. S., additional, Lee, V. M.-Y., additional, and Trojanowski, J. Q., additional

Published
2008
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38. Cognitive and motor assessment in autopsy-proven corticobasal degeneration

Author

Murray, R., primary, Neumann, M., additional, Forman, M. S., additional, Farmer, J., additional, Massimo, L., additional, Rice, A., additional, Miller, B. L., additional, Johnson, J. K., additional, Clark, C. M., additional, Hurtig, H. I., additional, Gorno-Tempini, M. L., additional, Lee, V. M.-Y., additional, Trojanowski, J. Q., additional, and Grossman, M., additional

Published
2007
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39. DLB and PDD boundary issues

Author

Lippa, C. F., primary, Duda, J. E., additional, Grossman, M., additional, Hurtig, H. I., additional, Aarsland, D., additional, Boeve, B. F., additional, Brooks, D. J., additional, Dickson, D. W., additional, Dubois, B., additional, Emre, M., additional, Fahn, S., additional, Farmer, J. M., additional, Galasko, D., additional, Galvin, J. E., additional, Goetz, C. G., additional, Growdon, J. H., additional, Gwinn-Hardy, K. A., additional, Hardy, J., additional, Heutink, P., additional, Iwatsubo, T., additional, Kosaka, K., additional, Lee, V. M.-Y., additional, Leverenz, J. B., additional, Masliah, E., additional, McKeith, I. G., additional, Nussbaum, R. L., additional, Olanow, C. W., additional, Ravina, B. M., additional, Singleton, A. B., additional, Tanner, C. M., additional, Trojanowski, J. Q., additional, and Wszolek, Z. K., additional

Published
2007
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45. Multicenter, placebo-controlled trial of cabergoline taken once daily in the treatment of Parkinson's disease

Author

Hutton, J.T., primary, Koller, W.C., additional, Ahlskog, J.E., additional, Pahwa, R., additional, Hurtig, H. I., additional, Stern, M. B., additional, Hiner, B. C., additional, Lieberman, A., additional, Pfeiffer, R. F., additional, Rodnitzky, R. L., additional, Waters, C. H., additional, Muenter, M. D., additional, Adler, C.H., additional, and Morris, J.L., additional

Published
1996
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48. A multicenter double‐blind placebo‐controlled trial of pergolide as an adjunct to sinemet® in Parkinson's disease

Author

Olanow, C. W., primary, Fahn, S., additional, Muenter, M., additional, Klawans, H., additional, Hurtig, H., additional, Stern, M., additional, Shoulson, I., additional, Kurlan, R., additional, Grimes, J. D., additional, Jankovic, J., additional, Hoehn, M., additional, Markham, C. H., additional, Duvisin, R., additional, Reinmuth, O., additional, Leonard, H. A., additional, Ahlskog, E., additional, Feldman, R., additional, Hershey, L., additional, and Yahr, M. D., additional

Published
1994
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