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Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy
Open accessAbstract
This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple‐author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state‐of‐the‐art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society
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“in addition, its effect seems to decrease over the years (33).”
From A Review on Wearable Technologies for Tremor Suppression (2021) · cites this paper as [33]
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“In the early 19th century, James Parkinson published his essay on “The Shaking Palsy,” in which he described in detail the clinical features (tremor, flexed posture, and festination) of a new disease with an insidious onset and a progressive disabling course called paralysis agitans; he was inspired by the observation…”
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APOE genotype regulates pathology and disease progression in synucleinopathy
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Self-citationEnergy Metabolism Decline in the Aging Brain—Pathogenesis of Neurodegenerative Disorders
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“Although these treatments reduce motor symptoms and improve the patient’s quality of life [7], clinical needs for new therapies to prevent, stop, or slow disease progression are not fully understood.”
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“Neuropathologically, Parkinson’s disease includes neuronal loss in the ventrolateral tier of the substantia nigra pars compacta and the corresponding striatal dopamine denervation and widespread intracellular α-synuclein accumulation [2, 53, 54].”
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BackgroundSelf-citationCerebral differences between dopamine-resistant and dopamine-responsive Parkinson’s tremor
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“This would fit the theory that tremor suppression is a threshold phenomenon with respect to the dose of levodopa required (Obeso et al., 2017).”
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The Pathology of Parkinson’s Disease and Potential Benefit of Dietary Polyphenols
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Innate and adaptive immune responses in Parkinson's disease
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Self-citationPeripheral Immune Profile and Neutrophil‐to‐Lymphocyte Ratio in Parkinson's Disease
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“Parkinson’s disease (PD) is one of the most common neurodegenerative disorders.(1) The etiopathogenesis of PD remains unclear, but current evidence points to neuroinflammation as a major contributor to the etiology and progression of neurodegeneration in PD.”
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The gut microbiome in Parkinson's disease: A culprit or a bystander?
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Gene therapy reduces Parkinson’s disease symptoms by reorganizing functional brain connectivity
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The heterogeneity of Parkinson’s disease
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Progressive parkinsonism in older adults is related to the burden of mixed brain pathologies
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“Hence, identifying clinical antecedents of PD prior to its clinical diagnosis, prodromal PD, offers the potential for early intervention and prevention.(5) While PD is uncommon, accumulating evidence suggests that parkinsonism, a heterogeneous disorder, may affect more than half of older adults by age 85.”
BackgroundL’Episcopo, F., Tirolo, C., Serapide, M. F., Caniglia, S., Testa, N., Leggio, L., Vivarelli, S., Iraci, N., Pluchino, S., & Marchetti, B. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00012 · Cited by 85
“…on dopamine replacement therapy, using the metabolic precursor of dopamine, L-DOPA, or dopamine receptor agonists, albeit they only temporally alleviate the motor symptoms without stopping the ongoing neurodegeneration (Olanow and Schapira, 2013; Obeso et al., 2017, for a comprehensive review).”
MethodHelley, M., Pinnell, J. R., Sportelli, C., & Tieu, K. (2017) · Frontiers in Genetics · doi:10.3389/fgene.2017.00177 · Cited by 98
“It has been proposed that this process involves a combination of selective expression of L-type Ca2+ channel leading to elevated cytosolic Ca2+, oxidized cytosolic dopamine, α-synuclein and the inherent long, highly branched axons of nigral dopaminergic neurons (Obeso et al., 2017).”
BackgroundCav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease
Benkert, J., Heß, S., Roy, S., Beccano-Kelly, D. A., Burkert, N., Duda, J., Simons, C., Patil, K., Gaifullina, A., Mannal, N., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12834-x · Cited by 99
Parkinson disease and the risk of epileptic seizures
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Chatterjee, D., Bhatt, M. A., Butler, D., Genst, E. D., Dobson, C. M., Messer, A. C., & Kordower, J. H. (2018) · npj Parkinson s Disease · doi:10.1038/s41531-018-0062-4 · Cited by 93
Self-citationCalcium, Bioenergetics, and Parkinson’s Disease
Zampese, E., & Surmeier, D. J. (2020) · Cells · doi:10.3390/cells9092045 · Cited by 79
“These neurons—whose degeneration is responsible for the core motor symptoms of Parkinson’s disease (PD) [6,7]—have large cytosolic oscillations in Ca2+ concentration ([Ca2+]).”
BackgroundSelf-citationSavitt, D., & Jankovic, J. J. (2019) · Drugs · doi:10.1007/s40265-019-01104-1 · Cited by 93
“The accumulation of misfolded α-syn into pathological aggregates is believed to play a central role in the pathogenesis of PD [2].”
BackgroundSelf-citationDevelopment of early diagnosis of Parkinson's disease: Illusion or reality?
Ugrumov, M. V. (2020) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13429 · Cited by 90
Deep brain stimulation-guided optogenetic rescue of parkinsonian symptoms
Valverde, S., Vandecasteele, M., Piette, C., Derousseaux, W., Gangarossa, G., Aristieta, A., Touboul, J. D., Degos, B., & Venance, L. (2020) · Nature Communications · doi:10.1038/s41467-020-16046-6 · Cited by 88
Basal lamina changes in neurodegenerative disorders
Nguyen, B., Bix, G., & Yao, Y. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00502-y · Cited by 75
“Typical symptoms of PD include resting tremor, gait disorders, and bradykinesia [303].”
BackgroundCell models for Alzheimer’s and Parkinson’s disease: At the interface of biology and drug discovery
Cetin, S., Knez, D., Gobec, S., Kos, J., & Pišlar, A. H. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112924 · Cited by 92
Diabetes, a Contemporary Risk for Parkinson’s Disease: Epidemiological and Cellular Evidences
Sergi, D., Renaud, J., Simola, N., & Martinoli, M. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00302 · Cited by 87
“Disease-causing duplications (Chartier-Harlin et al., 2004) and triplications (Singleton et al., 2003) of the SNCA gene were identified, and other genes were added in subsequent years (Obeso et al., 2017).”
BackgroundMadrid, J., & Benninger, D. H. (2020) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2020.108957 · Cited by 89
Amin, R., Quispe, C., Docea, A. O., Ydyrys, A., Kulbayeva, M., Durna Daştan, S., Calina, D., & Sharifi-Rad, J. (2022) · Neurochemistry International · doi:10.1016/j.neuint.2022.105376 · Cited by 74
Alpha-Synuclein as a Prominent Actor in the Inflammatory Synaptopathy of Parkinson’s Disease
Cardinale, A., Calabrese, V., de Iure, A., & Picconi, B. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126517 · Cited by 79
“The reduction of striatal dopaminergic neurons triggers motor symptoms that include bradykinesia, uncontrollable tremor at rest, postural impairment, and rigidity, which together characterise Parkinson’s disease (PD) as a movement disorder [1,2].”
BackgroundLin, K.-L., Lin, K.-J., Wang, P., Chuang, J., Lin, H., Chen, S., Chuang, Y., Huang, S., Tiao, M., Chen, J., et al. (2018) · Free Radical Research · doi:10.1080/10715762.2018.1489128 · Cited by 78
“Although highly efficacious pharmacological therapies have become available, none of these are curative and PD remains a progressive disorder [3,4].”
BackgroundThe misfolding mystery: α-synuclein and the pathogenesis of Parkinson's disease
Negi, S., Khurana, N., & Duggal, N. (2024) · Neurochemistry International · doi:10.1016/j.neuint.2024.105760 · Cited by 91
Sproviero, D., Gagliardi, S., Zucca, S., Arigoni, M., Giannini, M., Garofalo, M., Olivero, M., Dell’Orco, M., Pansarasa, O., Bernuzzi, S., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052737 · Cited by 76
“In PD degeneration of dopaminergic pigmented neurons in the substantia nigra (SN) and accumulation of α-synuclein protein, which is the main component of Lewy bodies (LBs), are the main features [5].”
BackgroundAnimal Models of Metabolic Disorders in the Study of Neurodegenerative Diseases: An Overview
Bem, A. F. D., Krolow, R., Farias, H. R., de Rezende, V. L., Gelain, D. P., Moreira, J. C. F., Duarte, J. M. N., & de Oliveira, J. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.604150 · Cited by 69
“Parkinson’s disease is the second most prevalent neurodegenerative disease after AD, and the most common movement disorder (Obeso et al., 2017).”
BackgroundThe role of T cells in the pathogenesis of Parkinson’s disease
Chen, Z., Chen, S., & Liu, J. (2018) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.08.002 · Cited by 81
Zhang, J., Culp, M. L., Craver, J., & Darley-Usmar, V. M. (2018) · Journal of Neurochemistry · doi:10.1111/jnc.14308 · Cited by 74
Insights into Parkinson’s disease from computational models of the basal ganglia
Humphries, M. D., Obeso, J. A., & Dreyer, J. K. (2018) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2017-315922 · Cited by 73
Self-citationTranscranial Temporal Interference Stimulation of the Right Globus Pallidus in Parkinson's Disease
Yang, C., Xu, Y.-X., Feng, X.-F., Wang, B., Du, Y., Wang, K., Lu, J.-J., Huang, L.-Y., Qian, Z., Wang, Z., et al. (2024) · Movement Disorders · doi:10.1002/mds.29967 · Cited by 65
Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases
Gong, L., Yin, J., Zhang, Y., Ren, H., Lou, Y., Jiang, H., Sun, L., Jia, J., & Zeng, X. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.914352 · Cited by 68
“Parkinson Disease (PD), one of the most common neurodegenerative diseases (Obeso et al., 2017), is characterized by the loss of dopaminergic neurons in the substantia nigra of midbrain (Zeng et al., 2014a).”
BackgroundCLR01 protects dopaminergic neurons in vitro and in mouse models of Parkinson’s disease
Bengoa-Vergniory, N., Faggiani, E., Ramos-Gonzalez, P., Kirkiz, E., Connor-Robson, N., Brown, L. V., Siddique, I., Li, Z., Vingill, S., Cioroch, M., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18689-x · Cited by 64
Clinical severity in Parkinson’s disease is determined by decline in cortical compensation
Johansson, M. E., Toni, I., Kessels, R. P. C., Bloem, B. R., & Helmich, R. C. G. (2023) · Brain · doi:10.1093/brain/awad325 · Cited by 69
“4,5 6-11 It remains unclear to what extent such compensatory processes, along with interindividual differences in their efficacy, contribute to clinical heterogeneity in Parkinson’s disease, over and above basal ganglia dysfunction.”
Neuroinflammation in Parkinson’s Disease: Triggers, Mechanisms, and Immunotherapies
Wang, T., Shi, C., Luo, H., Zheng, H., Fan, L., Tang, M., Su, Y., Yang, J., Mao, C., & Xu, Y. (2021) · The Neuroscientist · doi:10.1177/1073858421991066 · Cited by 69
Advances in Proteomic and Metabolomic Profiling of Neurodegenerative Diseases
Schuh, A. F. S., Bieger, A., Borelli, W. V., Portley, M. K., Awad, P. S., & Bandrés‐Ciga, S. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2021.792227 · Cited by 68
Nguyen, A. P. T., Tsika, E., Kelly, K., Levine, N. D., Chen, X., West, A. B., Boularand, S., Barnéoud, P., & Moore, D. J. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1922184117 · Cited by 72
“P disease (PD) typically occurs in a sporadic manner through a complex interaction between genetic risk, aging, and environmental exposure (1).”
A Review on Wearable Technologies for Tremor Suppression
Lora-Millan, J. S., Delgado-Oleas, G., Benito-León, J., & Rocon, E. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.700600 · Cited by 62
Lipidomics of Bioactive Lipids in Alzheimer’s and Parkinson’s Diseases: Where Are We?
Chiurchiù, V., Tiberi, M., Matteocci, A., Fazio, F., Siffeti, H., Saracini, S., Mercuri, N. B., & Sancesario, G. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116235 · Cited by 73
“One of the neuropathophysiological hallmarks of PD is characterized by the accumulation of α-synuclein (α-syn) and the formation of filamentous aggregates called “Lewy bodies” in the brainstem, limbic system, and cortical areas, leading to a progressive loss of dopaminergic neurons in the substantia nigra and striatum…”
BackgroundEspinoza, S., Scarpato, M., Damiani, D., Managò, F., Mereu, M., Contestabile, A., Peruzzo, O., Carninci, P., Santoro, C., Papaleo, F., et al. (2019) · Molecular Therapy · doi:10.1016/j.ymthe.2019.08.005 · Cited by 67
“Although familial PD (about 5% of the total cases) has been important to unveil the molecular pathways involved in neurodegeneration, most of the PD patients are sporadic.(2) Currently, no treatments are available that can slow or arrest neurodegeneration.”
BackgroundAn update on immune-based alpha-synuclein trials in Parkinson’s disease
Alfaidi, M., Barker, R. A., & Kuan, W. (2024) · Journal of Neurology · doi:10.1007/s00415-024-12770-x · Cited by 73
Lee, S.-B., Kim, Y.-J., Hwang, S., Son, H., Lee, S.-K., Park, K.-I., & Kim, Y.-G. (2022) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2022.01.011 · Cited by 60
Parkinson’s Disease-Related Genes and Lipid Alteration
Fais, M., Dore, A., Galioto, M., Galleri, G., Crosio, C., & Iaccarino, C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147630 · Cited by 69
“The etiology of PD is unknown, although older age and neurotoxins are established risk factors, and smoking appears to be protective [1].”
Backgroundα-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment
Karim, M. R., Liao, E. E., Kim, J., Meints, J. P., Martínez, H., Pletniková, O., Troncoso, J. C., & Lee, M. K. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00364-w · Cited by 66
Immunotherapy in Parkinson’s disease: Current status and future directions
Chatterjee, D., & Kordower, J. H. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104587 · Cited by 74
Self-citationAgerschou, E. D., Saridaki, T., Flagmeier, P., Galvagnion, C., Komnig, D., Nagpal, A., Gasterich, N., Heid, L. F., Prasad, V., Shaykhalishahi, H., et al. (2019) · eLife · doi:10.7554/elife.46112 · Cited by 70
Peripheral Inflammation Is Associated with Dopaminergic Degeneration in Parkinson's Disease
Muñoz‐Delgado, L., Labrador‐Espinosa, M. Á., Macías‐García, D., Jesús, S., Zamora, B. B., Fernández‐Rodríguez, P., Adarmes-Gómez, A. D., Castillo, M. I. R., Castro‐Labrador, S., Silva‐Rodríguez, J., et al. (2023) · Movement Disorders · doi:10.1002/mds.29369 · Cited by 61
“Following the neurodegeneration of the SNpc, a depletion of dopamine is observed through the nigrostriatal pathways, which is mainly responsible for the cardinal motor symptoms of PD.(2,3) The dopaminergic neurodegeneration associated with PD can be assessed in vivo by using [(123)I]FP-CIT single photon emission compu…”
BackgroundMethodResultInfluentialHill, B. G., Shiva, S., Ballinger, S. W., Zhang, J., & Darley-Usmar, V. M. (2019) · Biological Chemistry · doi:10.1515/hsz-2019-0268 · Cited by 66
Role of Microgliosis and NLRP3 Inflammasome in Parkinson’s Disease Pathogenesis and Therapy
de Araújo, F. M., Cuenca‐Bermejo, L., Fernández‐Villalba, E., Costa, S. L., da Silva, V. D. A., & Herrero, M. T. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-020-01027-6 · Cited by 63
Otomo, K., Perkins, J., Kulkarni, A. S., Stojanovic, S., Roeper, J., & Paladini, C. A. (2020) · Nature Communications · doi:10.1038/s41467-020-20041-2 · Cited by 54
Extracellular Vesicles as Novel Diagnostic and Prognostic Biomarkers for Parkinson’s Disease
Leggio, L., Paternò, G., Vivarelli, S., Falzone, G. G., Giachino, C., Marchetti, B., & Iraci, N. (2021) · Aging and disease · doi:10.14336/ad.2021.0527 · Cited by 55
“Of note, while providing a symptomatic relief [15, 23], these drugs do not modify the progressive neurodegenerative cell loss associated with PD, and in many cases, they result in debilitating side-effects [15].”
BackgroundPeripheral inflammatory immune response differs among sporadic and familial Parkinson’s disease
Muñoz‐Delgado, L., Macías‐García, D., Periñán, M. T., Jesús, S., Adarmes-Gómez, A. D., Bonilla‐Toribio, M., Buiza‐Rueda, D., Jiménez‐Jaraba, M. V., Zamora, B. B., Belloso, R. D., et al. (2023) · npj Parkinson s Disease · doi:10.1038/s41531-023-00457-5 · Cited by 62
The Gut Microbiome–Brain Crosstalk in Neurodegenerative Diseases
Ghezzi, L., Cantoni, C., Rotondo, E., & Galimberti, D. (2022) · Biomedicines · doi:10.3390/biomedicines10071486 · Cited by 61
“The main symptoms of PD are resting tremors, stiffness, bradykinesia, and postural instability [80].”
BackgroundJellinger, K. A. (2019) · Journal of Neural Transmission · doi:10.1007/s00702-019-02028-6 · Cited by 58
Cardiac Changes in Parkinson’s Disease: Lessons from Clinical and Experimental Evidence
Cuenca‐Bermejo, L., Almela, P., Navarro‐Zaragoza, J., Fernández‐Villalba, E., Cuello, A. M. G., Laorden, M. L., & Herrero, M. T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222413488 · Cited by 53
“Developed more than 50 years ago, this definition based on the motor condition is no longer an accurate description for PD; numerous works have evidenced that clinical manifestations of the disease go beyond the motor system and set up a complex scenario in which non-motor symptoms appear even years before the motor o…”
Background
Metadata
- Authors
- Obeso, J. A., Stamelou, M., Goetz, C. G., Poewe, W., Lang, A. E., Weintraub, D., Burn, D., Halliday, G. M., Bezard, E., Przedborski, S., Lehericy, S., Brooks, D. J., Rothwell, J. C., Hallett, M., DeLong, M. R., Marras, C., Tanner, C. M., Ross, G. W., Langston, J. W., Klein, C., Bonifati, V., Jankovic, J., Lozano, A. M., Deuschl, G., Bergman, H., Tolosa, E., Rodriguez‐Violante, M., Fahn, S., Postuma, R. B., Berg, D., Marek, K., Standaert, D. G., Surmeier, D. J., Olanow, C. W., Kordower, J. H., Calabresi, P., Schapira, A. H. V., & Stoessl, A. J.
- Affiliations
- Universidad San Pablo CEU (ES)
- Philipps University of Marburg (DE)
- Rush University Medical Center (US)
- Innsbruck Medical University (AT)
- University of Toronto (CA)
- Mental Illness Research, Education and Clinical Centers (US)
- Newcastle University (GB)
- The University of Sydney (AU)
- Université de Bordeaux Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives Bordeaux France
- Columbia University Irving Medical Center (US)
- Institut du Cerveau et de la Moelle épinière – ICM, Centre de NeuroImagerie de Recherche – CENIR Sorbonne Universités UPMC Univ Paris 06, Inserm U1127, CNRS UMR 7225 Paris France
- Aarhus University (DK)
- UCL Queen Square Institute of Neurology (GB)
- National Institutes of Health (US)
- Emory University (US)
- San Francisco VA Medical Center (US)
- VA Pacific Islands Health Care System (US)
- Parkinson's Institute and Clinical Center (US)
- University of Lübeck (DE)
- Erasmus MC (NL)
- Baylor College of Medicine (US)
- Christian-Albrechts-Universität zu Kiel (DE)
- Hebrew University of Jerusalem (IL)
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Movement Disorders Clinic Clinical Neurodegenerative Research Unit Mexico City Mexico
- Montreal General Hospital (CA)
- Institute for Neurodegenerative Disorders (US)
- University of Alabama at Birmingham (US)
- Northwestern University (US)
- Icahn School of Medicine at Mount Sinai (US)
- University of Perugia (IT)
- Vancouver Coastal Health (CA)
- Corresponding author
- Obeso, J.A.
- ORCID
- Obeso, J.A.
- Stamelou, M.
- Goetz, C.G.
- Poewe, W.
- Lang, A.E.
- Weintraub, D.
- Burn, D.
- Halliday, G.M.
- Przedborski, S.
- Brooks, D.J.
- Rothwell, J.C.
- Hallett, M.
- DeLong, M.R.
- Marras, C.
- Tanner, C.M.
- Klein, C.
- Bonifati, V.
- Jankovic, J.
- Lozano, A.M.
- Deuschl, G.
- Bergman, H.
- Tolosa, E.
- Rodriguez‐Violante, M.
- Postuma, R.B.
- Berg, D.
- Marek, K.
- Standaert, D.G.
- Surmeier, D.J.
- Olanow, C.W.
- Kordower, J.H.
- Calabresi, P.
- Schapira, A.H.V.
- Stoessl, A.J.
- Venue
- Movement Disorders
- Publisher
- Wiley
- Published
- 2017-09
- Volume
- 32
- Issue
- 9
- Pages
- 1264-1310
- ISSN
- 0885-3185 (ISSN-L)
- 1531-8257
- PMC
- PMC5685546
- OpenAlex
- W2753051298
- Cited by
- 859
- References
- 308
- Citations by year
- 2026: 78 · 2025: 88 · 2024: 90 · 2023: 116 · 2022: 115 · 2021: 128 · 2020: 104 · 2019: 82 · 2018: 50 · 2017: 6
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Movement Disorders (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- National Institute of Neurological Disorders and Stroke (P50NS053488, R01NS034696)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neurology and Historical Studies
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Keywords
- Parkinson's disease, history of Parkinson's disease, James Parkinson, etiopathogenesis, pathophysiology, symptomatic treatment, disease progression, future research directions
- MeSH terms
- Anniversaries and Special Events, Humans, Parkinson Disease, History, 19th Century, History, 20th Century, History, 21st Century
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