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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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“More rapid progression of all clinical features was predicted by the presence of REM behavioral disorder, mild cognitive impairment, and orthostatic hypotension in another.(29) To date, PD subtypes have been characterized on the basis of readily apparent and evaluable clinical”
Self-citationProgressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons
Ekstrand, M. I., Terzioglu, M., Galter, D., Zhu, S., Hofstetter, C., Lindqvist, E., Thams, S., Bergstrand, A., Hansson, F. S., Trifunovic, A., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605208103 · Cited by 605
MR-guided focused ultrasound thalamotomy for essential tremor: a proof-of-concept study
Lipsman, N., Schwartz, M. L., Huang, Y., Lee, L., Sankar, T., Chapman, M., Hynynen, K., & Lozano, A. M. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70048-6 · Cited by 604
Self-citationMultiple hit hypotheses for dopamine neuron loss in Parkinson's disease
Sulzer, D. (2007) · Trends in Neurosciences · doi:10.1016/j.tins.2007.03.009 · Cited by 602 · cited 1×
“SNc dopaminergic neurons also have the added liability of using dopamine as a neurotransmitter.(257) For example, the conjunction of dopamine, Ca(21) influx through plasma membrane Cav1 channels, and alphasynuclein disrupt chaperone mediated autophagy, promoting neurodegeneration.”
Marks, W. J., Ostrem, J. L., Verhagen, L., Starr, P. A., Larson, P. S., Bakay, R. A., Taylor, R., Cahn-Weiner, D. A., Stoessl, A. J., Olanow, C. W., et al. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(08)70065-6 · Cited by 596 · cited 1×
“Although some open-label trials reported benefit,(282) a double-blind trial did not meet its primary endpoint.(283) Ceregene Inc.”
Self-citationGlucocerebrosidase deficiency in substantia nigra of parkinson disease brains
Gegg, M. E., Burke, D. G., Heales, S., Cooper, J. A. D., Hardy, J., Wood, N. W., & Schapira, A. H. V. (2012) · Annals of Neurology · doi:10.1002/ana.23614 · Cited by 580
Self-citationMitochondria: The Next (Neurode)Generation
Schon, E. A., & Przedborski, S. (2011) · Neuron · doi:10.1016/j.neuron.2011.06.003 · Cited by 568 · cited 1×
“Second is the case of PINK1 and Parkin mutations that in humans cause recessive forms of familial PD and in flies major defects of mitochondria.(85) These observations reinvigorated the discussion of mitochondria defect in PD pathogenesis, but this time no longer from the angle of a deficit in bioenergics that have be…”
Self-citationRaz, A., Vaadia, E., & Bergman, H. (2000) · Journal of Neuroscience · doi:10.1523/jneurosci.20-22-08559.2000 · Cited by 567 · cited 1×
“In the past, theories of tremor genesis were focused on the idea that there are specific cell groups that have the tendency to oscillate and a mechanism that is related to the neurodegeneration synchronizes their oscillations.(202) However, it cannot be excluded that the oscillations are generated within brain network…”
Self-citationMosharov, E. V., Larsen, K. E., Kanter, E., Phillips, K. A., Wilson, K., Schmitz, Y., Krantz, D. E., Kobayashi, K., Edwards, R. H., & Sulzer, D. (2009) · Neuron · doi:10.1016/j.neuron.2009.01.033 · Cited by 548
Neurodegenerative Disorder Risk in Idiopathic REM Sleep Behavior Disorder: Study in 174 Patients
Iranzo, A., Fernández-Arcos, A., Tolosa, E., Serradell, M., Molinuevo, J. L., Valldeoriola, F., Gelpi, E., Vilaseca, I., Sánchez-Valle, R., Lladó, A., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0089741 · Cited by 548
Self-citationThe Onset of Nonmotor Symptoms in Parkinson's disease (The ONSET PD Study)
Pont‐Sunyer, C., Hotter, A., Gaig, C., Seppi, K., Compta, Y., Katzenschlager, R., Mas, N., Hofeneder, D., Brücke, T., Bayés, A., et al. (2015) · Movement Disorders · doi:10.1002/mds.26077 · Cited by 511 · cited 1×
“behavioral disorder, may even be the earliest disease manifestations, occurring years before any of the defining motor features are present.(19) Clearly, Parkin-”
Self-citationBerg, D., Postuma, R. B., Bloem, B. R., Chan, P., Dubois, B., Gasser, T., Goetz, C. G., Halliday, G. M., Hardy, J., Lang, A. E., et al. (2014) · Movement Disorders · doi:10.1002/mds.25844 · Cited by 502 · cited 1×
“”(1) Even with today’s insights from genetics and pathology, defining PD remains a challenge.(164) Moreover,”
Self-citationNeuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts
Jellinger, K. A. (2011) · Movement Disorders · doi:10.1002/mds.23795 · Cited by 480
Is alpha-synuclein in the colon a biomarker for premotor Parkinson’s disease? Evidence from 3 cases
Shannon, K. M., Keshavarzian, A., Dodiya, H. B., Jakate, S., & Kordower, J. H. (2012) · Movement Disorders · doi:10.1002/mds.25020 · Cited by 464 · cited 1×
“Indeed, alphasynuclein accumulation in the periphery has been well described,(5) with some studies suggesting the presence of LP in the colon prior to the onset of the classic motor features of PD.(267) Misfolded proteins could also form stochastically in a random fashion and lead to the accumulation of aggregated pro…”
Self-citationA large kindred with autosomal dominant Parkinson's disease
Golbe, L., Iorio, G. D., Bonavita, V., Miller, D. C., & Duvoisin, R. (1990) · Annals of Neurology · doi:10.1002/ana.410270309 · Cited by 463 · cited 1×
“At the same time, the evidence for genetic contributions was accumulating in the form of families with multiple affected members, including some families with pathologically proven Lewy-body PD that could be a familial disorder.(145) During the past 2 decades, genetic risk factors and causative genes have continued to…”
Caligiore, D., Pezzulo, G., Baldassarre, G., Bostan, A. C., Strick, P. L., Doya, K., Helmich, R. C. G., Dirkx, M. F., Houk, J. C., Jörntell, H., et al. (2016) · The Cerebellum · doi:10.1007/s12311-016-0763-3 · Cited by 454 · cited 2×
“Akineto-rigid and tremor-dominant forms of PD were associated with structural and functional changes predominating in the basal ganglia—cortical and cerebello-thalamocortical networks, respectively,(99) with tremor-related activity first arising in the internal part of the globus pallidus and propagating to the cerebe…”
Svennilson, E., Torvik, A., Lowe, R., & Leksell, L. (1960) · Acta Psychiatrica Scandinavica · doi:10.1111/j.1600-0447.1960.tb07606.x · Cited by 451 · cited 1×
“In 1992, Laitinen and colleagues(184) published a seminal paper on the reexamination of pallidotomy in the treatment of PD, which he had learned from Leksell 3 decades earlier.(185) The rediscovery and reintroduction of pallidotomy rekindled interest in surgery for PD fostered by a few studies in the MPTP monkey model…”
Neuropathology underlying clinical variability in patients with synucleinopathies
Halliday, G. M., Holton, J. L., Révész, T., & Dickson, D. W. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0852-9 · Cited by 447 · cited 2×
“For example, the most robust (and reciprocal) innervation of the SNc is onto striatal spiny projection neurons, which do not manifest LP in PD.(72,88) The appearance of Lewy-like pathology in striatal grafts(255) is also at odds with a simple synaptic spreading model because there”
Self-citationImaging amyloid deposition in Lewy body diseases
Gomperts, S. N., Rentz, D. M., Moran, E., Becker, J. A., Locascio, J. J., Klunk, W. E., Mathis, C. A., Elmaleh, D. R., Shoup, T., Fischman, A. J., et al. (2008) · Neurology · doi:10.1212/01.wnl.0000326146.60732.d6 · Cited by 443 · cited 1×
“The PET ligand (11)C-PIB, a neutral thioflavin-T analogue developed to image ß-amyloid plaques in dementia, has been employed to assess the prevalence of amyloid in PD patients.(124) Amyloid plaques can be detected with (11)C-PIB PET in a majority of dementia with Lewy-body cases, but only a minority of PDD or PD-MCI.”
Environmental risk factors and Parkinson's disease: An umbrella review of meta-analyses
Bellou, V., Belbasis, L., Tzoulaki, I., Εvangelou, Ε., & Ioannidis, J. P. A. (2015) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2015.12.008 · Cited by 443
Excessive daytime sleepiness and subsequent development of Parkinson disease
Abbott, R. D., Ross, G. W., White, L. R., Tanner, C. M., Masaki, K., Nelson, J. S., Curb, J. D., & Petrovitch, H. (2005) · Neurology · doi:10.1212/01.wnl.0000183056.89590.0d · Cited by 439 · cited 2×
“found that excessive napping or somnolence doubled the risk of PD.(230,234) Lead time is uncertain, but it is easily screened.”
Self-citationThe spectrum of nonmotor symptoms in early Parkinson disease
Khoo, T. K., Yarnall, A. J., Duncan, G. W., Coleman, S. Y., O'Brien, J. T., Brooks, D. J., Barker, R. A., & Burn, D. J. (2013) · Neurology · doi:10.1212/wnl.0b013e31827deb74 · Cited by 430
Self-citationEdison, P., Rowe, C. C., Rinne, J. O., Ng, S., Ahmed, I., Kemppainen, N. M., Villemagne, V. L., O'Keefe, G. J., Någren, K., Chaudhuri, К. R., et al. (2008) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2007.127878 · Cited by 428 · cited 2×
“In frankly demented PD patients, FDG PET shows reduced absolute levels of glucose utilization that targets the posterior cingulate, parietal, and temporal association areas.121 This pattern is present to a lesser extent in PD-MCI.122 Although the pattern of glucose hypometabolism in demented PD patients resembles that…”
Self-citationParkinson's disease: The quintessential neuropsychiatric disorder
Weintraub, D. A., & Burn, D. J. (2011) · Movement Disorders · doi:10.1002/mds.23664 · Cited by 422 · cited 1×
“The high prevalence of cognitive impairment and protean psychiatric complications has changed how we conceptualize PD.(47,48) This has manifested itself in the recently proposed revised clinical diagnostic criteria,(17,49) which allows for dementia to be a comorbid condition at the time of diagnosis.”
Self-citationFDG PET in the differential diagnosis of parkinsonian disorders
Eckert, T., Barnes, A., DHAWAN, V. M., Frucht, S. J., Gordon, M. F., Feigin, A., & Eidelberg, D. (2005) · NeuroImage · doi:10.1016/j.neuroimage.2005.03.012 · Cited by 418
Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor
Helmich, R. C., Janssen, M. J. R., Oyen, W. J. G., Bloem, B. R., & Toni, I. (2011) · Annals of Neurology · doi:10.1002/ana.22361 · Cited by 417 · cited 2×
“Further activation studies using tremor intensity as a measure to correlate the blood-oxygen-level dependent effect on MRI have shown that tremor onset is best correlated with a network within the basal ganglia (switching on tremor), whereas the tremor severity (dimmer of tremor) is related to the cerebello-cortical n…”
Pathological α‐synuclein in gastrointestinal tissues from prodromal Parkinson disease patients
Stokholm, M. G., Danielsen, E. H., Hamilton‐Dutoit, S. J., & Borghammer, P. (2016) · Annals of Neurology · doi:10.1002/ana.24648 · Cited by 415 · cited 1×
“A recent Danish study examined gastrointestinal biopsy samples from a national database in patients who eventually developed PD.(238) They documented increased phosphorylated synuclein staining in those destined to develop PD; 45% of prodromal PD samples were positive (median interval 5 7 years before PD diagnosis), c…”
A controlled trial of antidepressants in patients with Parkinson disease and depression
Menza, M. A., Dobkin, R. D., Marín, H., Mark, M. H., Gara, M. A., Buyske, S. G., Bienfait, K., & Dicke, A. (2008) · Neurology · doi:10.1212/01.wnl.0000336340.89821.b3 · Cited by 411
Resting state functional connectivity of the striatum in Parkinson’s disease
Hacker, C. D., Perlmutter, J. S., Criswell, S. R., Ances, B. M., & Snyder, A. Z. (2012) · Brain · doi:10.1093/brain/aws281 · Cited by 408
de la Fuente‐Fernández, R. (2004) · Brain · doi:10.1093/brain/awh290 · Cited by 404
Self-citationParkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion‐Like Disorder?
Olanow, C. W., & Brundin, P. (2013) · Movement Disorders · doi:10.1002/mds.25373 · Cited by 404 · cited 1×
“Importantly, the prion hypothesis identifies a series of novel targets and candidate therapeutic interventions that might prevent the formation or facilitate the clearance of misfolded alpha-synuclein and thereby have disease-modifying effects.(268,269)”
Self-citationMagnetic resonance imaging markers of Parkinson's disease nigrostriatal signature
Péran, P., Cherubini, A., Assogna, F., Piras, F., Quattrocchi, C., Peppe, A., Celsis, P., Rascol, O., Démonet, J.-F., Stefani, A., et al. (2010) · Brain · doi:10.1093/brain/awq212 · Cited by 399
Respondek, G., Stamelou, M., Kurz, C., Ferguson, L. W., Rajput, A. H., Chiu, W. Z., Swieten, J. C. V., Troakes, C., Sarraj, S. A., Gelpí, E., et al. (2014) · Movement Disorders · doi:10.1002/mds.26054 · Cited by 395
Self-citationMetabolic brain networks in neurodegenerative disorders: a functional imaging approach
Eidelberg, D. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2009.06.003 · Cited by 389 · cited 4×
“degree of expression correlates with the degree of motor disability.(107) The PDRP normalizes after successful treatment with both dopaminergic drugs or DBS.”
InfluentialAccuracy of clinical diagnosis of Parkinson disease: A systematic review and meta-analysis
Jellinger, K., Logroscino, G., Rizzo, G., Copetti, M., Arcuti, S., Martino, D., & Fontana, A. (2016) · Neurology · doi:10.1212/wnl.0000000000002876 · Cited by 384 · cited 2×
“Imaging may be helpful, in particular if specific MRI changes precede satisfaction of clinical criteria,(42) but accuracy of diagnosis based on MRI findings and PET/single-photon emission computerized tomography (SPECT) imaging is not higher than clinical expertise in clinicopathological studies.(33) Drug-induced park…”
Penney, J., Oakes, D., Shoulson, I., Fahn, S., Lang, A., Langston, J., LeWitt, P., Olanow, C., Tanner, C., & Kieburtz, K. (1996) · Annals of Neurology · doi:10.1002/ana.410390107 · Cited by 380 · cited 1×
“5 months of levodopa therapy half experienced a wearing-off phenomenon.(179) In the ELLDOPA study, 16.”
Self-citationHoltzman, R. M. (2013) · História, Ciências, Saúde: Manguinhos · doi:10.1590/s0104-59702013000500001 · Cited by 376
Snow, B., Tooyama, I., Mcgeer, E., Yamada, T., Calne, D., Takahashi, H., & Kimura, H. (1993) · Annals of Neurology · doi:10.1002/ana.410340304 · Cited by 367
Pooled analysis of tobacco use and risk of Parkinson disease.
Ritz, B., Ascherio, A., Checkoway, H., Marder, K., Nelson, L., Rocca, W., Ross, G., Strickland, D., den Eeden, S. K. V., & Gorell, J. (2007) · Archives of Neurology · doi:10.1001/archneur.64.7.990 · Cited by 366 · cited 2×
“Smokeless tobacco users are also at lower risk of PD, indirectly supporting an effect of nicotine.(151) Variants in several genes have been reported to modify the effect of smok-”
Self-citationVitamin K 2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
Vos, M. H., Esposito, G., Edirisinghe, J. N., Vilain, S., Haddad, D., Slabbaert, J. R., Meensel, S. V., Schaap, O., Strooper, B. D., Meganathan, R., et al. (2012) · Science · doi:10.1126/science.1218632 · Cited by 366 · cited 1×
“Drosophila identified vitamin K2 as a suppressor of the PINK1 mutant phenotype, which functions as an electron carrier molecule in mitochondria leading to improved ATP production.(167) It has thus been hypothesized that stratifying PD patients according to different degrees of mitochondrial dysfunction based on their…”
Jellinger, K. A. (1999) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-6360-3_1 · Cited by 359 · cited 1×
“One of the main claims of earlier papers was that the cells of the Area 8 close to the SN and caudal to the red nucleus are preferentially degenerating.(198,199) This is in keeping with the suggested differential pattern of degeneration between tremor-dominant patients and akinesiadominant patients.”
Midbrain iron content in early Parkinson disease
Martin, W. R. W., Wieler, M., & Gee, M. (2008) · Neurology · doi:10.1212/01.wnl.0000286384.31050.b5 · Cited by 355 · cited 2×
“Increased iron content may predominate in the lateral segments of the SN and in some studies correlated with the UPDRS motor score.(88) A number of studies have reported altered diffusion properties in the SN, characterized by reduced fractional anisotropy, but the large variability of the results question the reliabi…”
Postuma, R., Lang, A.-E., Gagnon, J., Pelletier, A., & Montplaisir, J. (2012) · Brain : a journal of neurology · doi:10.1093/brain/aws093 · Cited by 352 · cited 1×
“Whereas redundancy is common in many neurodegenerative disorders, a unique advantage of PD is that it has a nonmotor prodrome.(221) Arguably one of the most important new insights during the past 20 years is that PD can start outside of the SNpc.”
Self-citationDopamine Agonist Withdrawal Syndrome in Parkinson Disease
Rabinak, C. A., & Nirenberg, M. J. (2010) · Archives of Neurology · doi:10.1001/archneurol.2009.294 · Cited by 347 · cited 2×
“Indeed, DBS is increasingly used as a treatment to address the problem of reducing dopaminergic drugs without inducing motor deterioration in patients with ICD.(62) Cognitive impairment (particularly impaired verbal fluency) post-DBS surgery has consistently been reported, with some evidence that these effects are pre…”
Complex I and Parkinson's Disease
Greenamyre, J. T., Sherer, T., Betarbet, R. S., & Panov, A. V. (2001) · IUBMB Life · doi:10.1080/15216540152845939 · Cited by 343 · cited 2×
“drial electron transport chain) is diminished in the SN, suggesting mitochondrial damage.(247) Third, in PD”
Use of ibuprofen and risk of Parkinson disease
Gao, X., Chen, H., Schwarzschild, M. A., & Ascherio, A. (2011) · Neurology · doi:10.1212/wnl.0b013e31820f2d79 · Cited by 339
A randomized, double-blind, placebo-controlled trial of antidepressants in Parkinson disease
Richard, I., McDermott, M. P., Kurlan, R., Lyness, J. M., Como, P. G., Pearson, N., Factor, S. A., Juncos, J. L., Ramos, C. S., Brodsky, M., et al. (2012) · Neurology · doi:10.1212/wnl.0b013e3182516244 · Cited by 335
Dopamine Is Required for the Neural Representation and Control of Movement Vigor
Panigrahi, B., Martin, K. A., Li, Y., Graves, A. R., Vollmer, A., Olson, L., Mensh, B. D., Karpova, A. Y., & Dudman, J. T. (2015) · Cell · doi:10.1016/j.cell.2015.08.014 · Cited by 330 · cited 1×
“The dramatic and immediate beneficial effects of ablation and DBS of GPi in both primate models and patients with PD and dystonia, with little or no impairment of movement or behavior, argues against an essential role of the basal ganglia in the on-line control of movement and favors the view, now strongly supported b…”
Games, D., Valera, E., Spencer, B. J., Rockenstein, E. M., Mante, M., Adame, A., Patrick, C., Ubhi, K. K., Nuber, S., Sacayon, P., et al. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.5314-13.2014 · Cited by 329
Nonmotor features of Parkinson's disease subtypes
Marras, C., & Chaudhuri, К. R. (2016) · Movement Disorders · doi:10.1002/mds.26510 · Cited by 327
Self-citationExposure to pesticides or solvents and risk of Parkinson disease
Pezzoli, G., & Cereda, E. (2013) · Neurology · doi:10.1212/wnl.0b013e318294b3c8 · Cited by 327
McNeill, A., Magalhães, J., Shen, C., Chau, K., Hughes, D. A., Mehta, A. B., Foltynie, T., Cooper, J. A. D., Abramov, A. Y., Gegg, M. E., et al. (2014) · Brain · doi:10.1093/brain/awu020 · Cited by 324
Self-citationIranzo, Á., Valldeoriola, F., Lomeña, F., Molinuevo, J., Serradell, M., Salamero, M., Cot, A., Ros, D., Pavía, J., Santamaria, J., et al. (2011) · Lancet Neurology · doi:10.1016/s1474-4422(11)70152-1 · Cited by 319
Self-citationHall, H., Reyes, S., Landeck, N., Bye, C. R., Leanza, G., Double, K. L., Thompson, L. H., Halliday, G. M., & Kirik, D. (2014) · Brain · doi:10.1093/brain/awu193 · Cited by 315 · cited 1×
“However, the pattern of dopamine cell loss in the SN is distinctive for PD, with the most severe loss found in the ventrolateral region of the SN, whereas dopaminergic neurons in the nearby ventral tegmental area are nearly entirely spared.(65) Moderate to severe loss of the pigmented dopamine neurons in the SN is fou…”
Self-citationPathophysiology of Parkinson's disease: From clinical neurology to basic neuroscience and back
Bergman, H., & Deuschl, G. (2002) · Movement Disorders · doi:10.1002/mds.10140 · Cited by 314 · cited 1×
“Several hypotheses have been put forward.(205,206) The first suggestion is the thalamic oscillator hypothesis assuming that thalamic cells oscillate and drive PD tremor, probably through the motor cortex.”
Self-citationGarcía-Lorenzo, D., Santos, C. L.-D., Ewenczyk, C., Leu‐Semenescu, S., Galléa, C., Quattrocchi, G., Lobo, P. P., Poupon, C., Benali, H., Arnulf, I., et al. (2013) · Brain · doi:10.1093/brain/awt152 · Cited by 314
Neumann, W., Degen, K., Schneider, G., Brücke, C., Huebl, J., Brown, P., & Kühn, A. (2016) · Movement Disorders · doi:10.1002/mds.26759 · Cited by 312
Cognitive-Behavioral Therapy for Depression in Parkinson's Disease: A Randomized, Controlled Trial
Dobkin, R. D., Menza, M., Allen, L. A., Gara, M. A., Mark, M. H., Tiu, J., Bienfait, K. L., & Friedman, J. (2011) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2011.10111669 · Cited by 310 · cited 1×
“In addition, cognitive behavior therapy has been shown to be efficacious,(5) but its role in the management of cognitive impairment in PD is not yet cleart.(56) Among the disorders of affect, both anxiety and apathy in PD have received less attention than depression despite their frequent occurrence (30%-40% for each…”
Lectures on the diseases of the nervous system, delivered at La Salpêtrière, 2nd ed.
Charcot, J., & Sigerson, G. (n.d.) · doi:10.1037/12839-000 · Cited by 309
A critical appraisal of the pathogenic protein spread hypothesis of neurodegeneration
Walsh, D. M., & Selkoe, D. J. (2016) · Nature reviews. Neuroscience · doi:10.1038/nrn.2016.13 · Cited by 301 · cited 1×
“Although cell-to-cell transmission of alpha-synuclein has been demonstrated in both cell culture and animal models, the exact sequence and molecular mechanisms of propagation of PD’s neuropathology throughout the human brain remain elusive.(157) PARK-LRRK2.”
Olanow, C. W., Bartus, R. T., Baumann, T. L., Factor, S. A., Boulis, N. M., Stacy, M. A., Turner, D. A., Marks, W. J., Larson, P., Starr, P. A., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24436 · Cited by 287 · cited 1×
“However, multiple clinical trials, including 2 phase II trials, failed to meet the primary endpoint.(284) Uncertainty remains about the potential efficacy of trophic factors in PD.”
Self-citationAutophagy and A lpha‐ S ynuclein: R elevance to P arkinson's D isease and R elated S ynucleopathies
Xilouri, M., Brekk, O. R., & Stefanis, L. (2016) · Movement Disorders · doi:10.1002/mds.26477 · Cited by 280 · cited 1×
“Genetic mutations affecting both have been implicated in PD.(245,246)”
Diógenes, M. J., Dias, R. B., Rombo, D. M., Miranda, H. V., Maiolino, F., Guerreiro, P. S., Näsström, T., Franquelim, H. G., Oliveira, L. M. A., Castanho, M. A. R. B., et al. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.0234-12.2012 · Cited by 274
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Self-citationNandhagopal, R., Kuramoto, L., Schulzer, M., Mak, E., Cragg, J. J., Lee, C. S., McKenzie, J., McCormick, S., Samii, A., Troiano, A. R., et al. (2009) · Brain · doi:10.1093/brain/awp209 · Cited by 270 · cited 1×
“in early (or presumably presymptomatic) phases of disease.(112) Reverse extrapolation of the exponential defining this pattern of decline suggests that vesicular monoamine transporter type 2 binding declines first (more than 15 years prior to disease onset), followed by a decline in DAT binding (some 10-15 years prior…”
Self-citationClinical spectrum of levodopa‐induced complications
Aquino, C., & Fox, S. H. (2014) · Movement Disorders · doi:10.1002/mds.26125 · Cited by 269 · cited 1×
“Motor complications (ie, fluctuations and dyskinesias) associated with chronic levodopa therapy represent a major challenge in the treatment of patients with PD.(177,178) In a large, prospective study, 29% of 352 patients originally enrolled in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP…”
Mure, H., Hirano, S., Tang, C. C., Isaias, I. U., Antonini, A., Ma, Y., DHAWAN, V. M., & Eidelberg, D. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2010.09.028 · Cited by 264
A new dynamic model of the cortico-basal ganglia loop
Nambu, A. (2004) · Progress in brain research · doi:10.1016/s0079-6123(03)43043-4 · Cited by 263 · cited 1×
“The STN also receives input from the cortex, the “hyperdirect” pathway, which is postulated to play a role in the cancellation of an inappropriate movement.(141) It is likely that other structures and feedback loops, such as those involving the pedunculopontine nucleus (PPN) and the Centromedianum (CM) also contribute…”
The thalamostriatal system in normal and diseased states
Smith, Y., Galván, A., Ellender, T. J., Doig, N. M., Villalba, R. M., Huerta-Ocampo, I., Wichmann, T., & Bolam, J. P. (2014) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2014.00005 · Cited by 259 · cited 1×
“In addition, the CMstriatal projection has been found to degenerate in PD patients.(142) In parkinsonian animals, lesioning of the PPN, which may include the brainstem locomotor region, has been associated with akinesia, whereas increased PPN activity is associated with an amelioration of parkinsonism.”
Disease‐modifying strategies for Parkinson's disease
Kalia, L. V., Kalia, S. K., & Lang, A. E. (2015) · Movement Disorders · doi:10.1002/mds.26354 · Cited by 254 · cited 1×
“lnflammation is a major component of PD pathogenesis, and a clinical trial using Pioglitazone, a peroxisome proliferator-activated receptor-g agonist that reduces proinflammatory cytokines and modulates mitochondrial biogenesis, was performed.(70,273) However, this trial failed to meet its primary endpoint as well.”
Self-citationPatterns and stages of α-synucleinopathy
ZACCAI, J. H., Brayne, C., McKeith, I. G., Matthews, F. E., & Ince, P. G. (2008) · Neurology · doi:10.1212/01.wnl.0000306697.48738.b6 · Cited by 249
Levodopa‐induced dyskinesias in Parkinson's disease: Clinical and pharmacological classification
Luquin, M., Scipioni, O., Vaamonde, J., Gershanik, O., & Obeso, J. (1992) · Movement Disorders · doi:10.1002/mds.870070204 · Cited by 246 · cited 2×
“It is typically manifested by the onset of unilateral leg stereotypy followed by other abnormal involuntary movements involving the ipsilateral and then contralateral body within 10 to 15 minutes after ingesting levodopa, lasting about 15 minutes, after which time there is improvement of parkinsonism for several hours…”
Self-citationInosine to Increase Serum and Cerebrospinal Fluid Urate in Parkinson Disease
Schwarzschild, M. A., Ascherio, A., Beal, M. F., Cudkowicz, M., Curhan, G. C., Hare, J. M., Hooper, D. C., Kieburtz, K. D., Macklin, E. A., Oakes, D., et al. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2013.5528 · Cited by 246
Self-citationSerotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson’s disease patients
Politis, M., Wu, K., Loane, C., Brooks, D. J., Kiferle, L., Turkheimer, F., Bain, P. G., Molloy, S., & Piccini, P. P. (2014) · Journal of Clinical Investigation · doi:10.1172/jci71640 · Cited by 245 · cited 1×
“Levodopa-induced dyskinesias thus likely reflect an aberrant pattern of dopamine release; this may arise from conversion of levodopa to dopamine in surviving serotonergic neurons, as suggested in animal models and supported by imaging studies.(116) Dyskinesias have also been linked to reduced opioid receptor,(117) inc…”
Self-citationAsymmetric pedunculopontine network connectivity in parkinsonian patients with freezing of gait
Fling, B. W., Cohen, R. G., Mancini, M., Nutt, J. G., Fair, D. A., & Horak, F. B. (2013) · Brain · doi:10.1093/brain/awt172 · Cited by 244
Kalaitzakis, M. E., Graeber, M. B., Gentleman, S., & Pearce, R. K. B. (2007) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2007.00923.x · Cited by 243 · cited 1×
“First, although all PD brains manifest LP in a stereotyped collection of nuclei, there are many deviations from the original staging model of Braak and colleagues, arguing against a stereotyped spread of LP through the brain.(252,253) Second, the distribution of LP in PD does not conform to a simple connectome rule.”
Postuma, R. B., Gagnon, J., Vendette, M., Desjardins, C., & Montplaisir, J. Y. (2010) · Annals of Neurology · doi:10.1002/ana.22282 · Cited by 242
Self-citationCalcium, Bioenergetics, and Neuronal Vulnerability in Parkinson's Disease
Surmeier, D. J., & Schumacker, P. T. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.r112.410530 · Cited by 240 · cited 1×
“The following 3 uncommon traits are shared by the small collection of neurons at risk in PD: long, highly branched axons with many alphasynuclein enriched vesicular release sites; autonomous pacemaking activity that triggers a pronounced elevation in cytosolic Ca(21) concentration; and high basal mitochondrial oxidant…”
Self-citationMinor hallucinations occur in drug‐naive Parkinson's disease patients, even from the premotor phase
Pagonabarraga, J., Martinez‐Horta, S., Fernández de Bobadilla, R., Pérez, J., Ribosa‐Nogué, R., Marín, J., Pascual‐Sedano, B., García, C., Gironell, A., & Kulisevsky, J. (2016) · Movement Disorders · doi:10.1002/mds.26432 · Cited by 236 · cited 1×
“A recent study reported that the latter are common even in newly diagnosed, untreated patients.(58) Hallucinations were once thought to be almost exclusively visual, but auditory, tactile, and olfactory hallucinations are also relatively common.”
Depressive symptoms in PD correlate with higher 5-HTT binding in raphe and limbic structures
Politis, M., Wu, K., Loane, C., Turkheimer, F., Molloy, S., Brooks, D. J., & Piccini, P. P. (2010) · Neurology · doi:10.1212/wnl.0b013e3181feb2ab · Cited by 224
Self-citationRodríguez‐Oroz, M., López‐Azcárate, J., García‐García, D., Alegre, M., Toledo, J. B., Valencia, M., Guridi, J., Artieda, J., & Obeso, J. A. (2010) · Brain · doi:10.1093/brain/awq301 · Cited by 223 · cited 2×
“In PD patients who develop levodopa–induced dyskynesias (LIDs) and/or pathological impulsivity, a peak in the theta band is recorded in the STN.139 Although still controversial, it is widely believed that abnormal beta band synchrony and STN motor cortex coupling play a critical and important role in the production of…”
Self-citationAge‐specific progression of nigrostriatal dysfunction in Parkinson's disease
de la Fuente‐Fernández, R., Schulzer, M., Kuramoto, L., Cragg, J., Ramachandiran, N., Au, W. L., Mak, E., McKenzie, J., McCormick, S., Sossi, V., et al. (2011) · Annals of Neurology · doi:10.1002/ana.22284 · Cited by 222
Self-citationLongitudinal changes in free-water within the substantia nigra of Parkinson’s disease
Ofori, E., Pasternak, O., Planetta, P. J., Li, H., Burciu, R. G., Snyder, A. F., Lai, S., Okun, M. S., & Vaillancourt, D. E. (2015) · Brain · doi:10.1093/brain/awv136 · Cited by 222 · cited 1×
“For instance, new metrics allowing the characterization of neurite orientation dispersion and density or free water may be more sensitive to PD pathology in the nigra.(90) Reduced connectivity of the SN with the basal ganglia and thalamus were also evidenced in PD patients using tractography-based methods and resting…”
Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study
Bohnen, N. I., Koeppe, R. A., Minoshima, S., Giordani, B., Albin, R. L., Frey, K. A., & Kuhl, D. E. (2011) · Journal of Nuclear Medicine · doi:10.2967/jnumed.111.089946 · Cited by 217 · cited 2×
“Cholinergic terminal function in PD has been assessed with (11)C-NMP4A and (11)C-PMP PET, markers of acetylcholine esterase activity.(123,127) Nondemented PD patients showed posteriorly reduced cholinergic function in parietal and occipital cortex with (11)C-NMP4A PET, and this spreads to involve frontal cortex when d…”
Depression and subsequent risk of Parkinson disease
Gustafsson, H., Nordström, A., & Nordström, P. (2015) · Neurology · doi:10.1212/wnl.0000000000001684 · Cited by 217
Clinical correlates of raphe serotonergic dysfunction in early Parkinson's disease.
Qamhawi, Z., Towey, D., Shah, B., Pagano, G., Seibyl, J., Marek, K., Borghammer, P., Brooks, D., & Pavese, N. (2015) · Brain : a journal of neurology · doi:10.1093/brain/awv215 · Cited by 216 · cited 1×
“This has now been confirmed with (123)I-FP-CIT SPECT in a large group of de novo patients.(197) Interestingly, the raphe serotonin transporter availability was inversely correlated with rest tremor severity, and tremulous PD had less raphe serotonin transporter density but less severe striatal dopaminergic deficits th…”
Self-citationToward a redefinition of Parkinson's disease
Stern, M. B., Lang, A. E., & Poewe, W. H. (2012) · Movement Disorders · doi:10.1002/mds.24051 · Cited by 202
Self-citationEsposito, F., Tessitore, A., Giordano, A., Micco, R. D., Paccone, A., Conforti, R., Pignataro, G., Annunziato, L., & Tedeschi, G. (2013) · Brain · doi:10.1093/brain/awt007 · Cited by 202
Clinical correlates of levodopa-induced dopamine release in Parkinson disease
Pavese, N., Evans, A., Tai, Y. F., Hotton, G. R., Brooks, D., Lees, A., & Piccini, P. (2006) · Neurology · doi:10.1212/01.wnl.0000242888.30755.5d · Cited by 201
Self-citationPatterns of levodopa response in Parkinson's disease: a clinico-pathological study.
Kempster, P., Williams, D. R., Selikhova, M., Holton, J., Révész, T., & Lees, A. J. (2007) · Brain : a journal of neurology · doi:10.1093/brain/awm142 · Cited by 198
Functional connectivity in the basal ganglia network differentiates PD patients from controls
Szewczyk‐Królikowski, K., Menke, R., Rolinski, M., Duff, E. P., Salimi‐Khorshidi, G., Filippini, N., Zamboni, G., Hu, M. T. M., & Mackay, C. E. (2014) · Neurology · doi:10.1212/wnl.0000000000000592 · Cited by 197
Seven‐tesla magnetic resonance images of the substantia nigra in Parkinson disease
Kwon, D.-H., Kim, J.-M., Oh, S., Jeong, H., Park, S.-Y., Oh, E., Chi, J.-G., Kim, Y.-B., Jeon, B., & Cho, Z. (2012) · Annals of Neurology · doi:10.1002/ana.22592 · Cited by 192 · cited 2×
“This sign (called the dorsal nigral hyperintensity or DNH sign) has a diagnostic accuracy of more than 90%.(92) The second technique relies on the paramagnetic properties of neuromelanin, a pigment that is contained in the SN pars compacta (SNc).”
Science, medicine, and the future: Parkinson's disease
Schapira, A. H. V. (1999) · BMJ · doi:10.1136/bmj.318.7179.311 · Cited by 192 · cited 1×
“A third term, neurorescue, may be used when an intervention targets the adverse pathogenetic pathways directly and is capable not only of protecting neurons but also restoring their diminished function.(270) Medicine as practiced in the time of James Parkinson had no access to cures, although reference was often made…”
Self-citationPrecision medicine for disease modification in Parkinson disease
Espay, A. J., Brundin, P., & Lang, A. E. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2016.196 · Cited by 186 · cited 1×
“An important active research goal is to define methods of distinguishing subtypes at the earliest stages of the disease with future expectation that advances in precision medicine will allow the application of patient subtype-specific disease modification strategies.(32) The differential diagnosis of PD is relevant fo…”
Self-citationErro, R., Vitale, C., Amboni, M., Picillo, M., Moccia, M., Longo, K., Santangelo, G., Rosa, A. D., Allocca, R., Giordano, F., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0070244 · Cited by 185 · cited 1×
“Early urinary dysfunction characterized a “nonmotor dominant” subgroup and suggested a more malignant course in one study.(28) More rapid progression of all clinical features was predicted by the presence of REM behavioral disorder, mild cognitive impairment, and orthostatic hypotension in another.”
Environmental Toxins and Parkinson's Disease
Ratner, M. H., & Feldman, R. (2005) · doi:10.1201/9780203508596.sec2 · Cited by 185 · cited 3×
“In some cases, the adverse effect of a pesticide is increased in persons with genetically determined altered function of toxicant handling.(148) Conversely, other behaviors appear to protect against the adverse effects of pesticide exposure.”
Caffeine and risk of Parkinson’s disease in a large cohort of men and women
Palacios, N., Gao, X., McCullough, M. L., Schwarzschild, M. A., Shah, R., Gapstur, S., & Ascherio, A. (2012) · Movement Disorders · doi:10.1002/mds.25076 · Cited by 185 · cited 2×
“Coffee and tea drinking as well as caffeine consumption are also associated with a lower risk of PD.(153)”
Why have we failed to achieve neuroprotection in Parkinson's disease?
Olanow, C. W., Kieburtz, K. D., & Schapira, A. H. V. (2009) · Annals of Neurology · doi:10.1002/ana.21461 · Cited by 184 · cited 1×
“However, there remain many obstacles both to identifying therapies capable of modifying the natural course of PD and to testing their efficacy in clinical trials.(295) Using a combination of therapies targeting multiple pathogenetic pathways simultaneously offers some attraction.”
Self-citationPiccini, P., Weeks, R., & Brooks, D. (1997) · Annals of Neurology · doi:10.1002/ana.410420508 · Cited by 183
Self-citationLysosomal Dysfunction and α‐Synuclein Aggregation in Parkinson's Disease: Diagnostic Links
Moors, T. E., Paciotti, S., Chiasserini, D., Calabresi, P., Parnetti, L., Beccari, T., & van de Berg, W. D. J. (2016) · Movement Disorders · doi:10.1002/mds.26562 · Cited by 181 · cited 1×
“Genetic mutations affecting both have been implicated in PD.(245,246)”
Self-citationPramipexole in patients with early Parkinson's disease (PROUD): a randomised delayed-start trial
Schapira, A., McDermott, M., Barone, P., Comella, C., Albrecht, S., Hsu, H., Massey, D., Mizuno, Y., Poewe, W., Rascol, O., et al. (2013) · Lancet Neurology · doi:10.1016/s1474-4422(13)70117-0 · Cited by 179 · cited 1×
“Other trials(70) used imaging techniques to assess neuroprotection as the primary endpoint as opposed to clinical disease modification, and although initial studies suggested that pramipexole (CALM-PD) and ropinirole (REAL-PD) studies slowed the loss of dopamine imaging markers relative to levodopa, these changes are…”
Self-citationLessons from the rotenone model of Parkinson's disease
Greenamyre, J. T., Cannon, J. R., Drolet, R. E., & Mastroberardino, P. G. (2010) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2009.12.006 · Cited by 179 · cited 1×
“another environmental toxin associated with PD, also is a mitochondrial poison.(247,248) Second, in PD brains,”
Vilas, D., Iranzo, Á., TOLOSA, E. S., Aldecoa, I., Berenguer, J., Vilaseca, I., Martí, C. D., Serradell, M., Lomeña, F., Alós, L., et al. (2016) · The Lancet Neurology · doi:10.1016/s1474-4422(16)00080-6 · Cited by 179 · cited 1×
“A recent study in idiopathic RBD found synuclein deposition in 8/9 submandibular gland samples (compared to none in controls).(239) If specificity issues can be resolved, there is considerable future promise for tissue biopsy in early detection of PD.”
Self-citationEggers, C., Kahraman, D., Fink, G., Schmidt, M. C., & Timmermann, L. (2011) · Movement Disorders · doi:10.1002/mds.23468 · Cited by 175
α-Synuclein-Based Animal Models of Parkinson's Disease: Challenges and Opportunities in a New Era
Visanji, N. P., Brotchie, J. M., Kalia, L. V., Koprich, J. B., Tandon, A., Watts, J. C., & Lang, A. E. (2016) · Trends in Neurosciences · doi:10.1016/j.tins.2016.09.003 · Cited by 174
Self-citationLigation of the anterior choroidal artery for involuntary movements-parkinsonism
Cooper, I. S. (1953) · Psychiatric quarterly · doi:10.1007/bf01562492 · Cited by 171 · cited 1×
“Surgery was aborted and the patient awoke with no deficits and with clear clinical benefit on the basis of the resulting ischemic lesion of the subthalamic nucleus, the globus pallidus, and their projections.(182) This led to a flurry of arterial ligation surgeries, but the variability and unpredictability of outcomes…”
Mild cognitive impairment as a risk factor for Parkinson's disease dementia
Hoogland, J., Boel, J. A., de Bie, R. M. A., Geskus, R. B., Schmand, B. A., Dalrymple‐Alford, J. C., Marras, C., Adler, C. H., Goldman, J. G., Tröster, A. I., et al. (2017) · Movement Disorders · doi:10.1002/mds.27002 · Cited by 171
Self-citationMeyers, R., Fry, W., Fry, F. J., Dreyer, L. L., Schultz, D. F., & Noyes, R. F. (1959) · Journal of Neurosurgery · doi:10.3171/jns.1959.16.1.0032 · Cited by 167
Biomarkers for dementia and mild cognitive impairment in Parkinson's disease
Delgado‐Alvarado, M., Gago, B., Navalpotro‐Gómez, I., Jiménez‐Urbieta, H., & Rodríguez-Oroz, M. C. (2016) · Movement Disorders · doi:10.1002/mds.26662 · Cited by 166 · cited 1×
“PD with dementia when compared with PD-MCI and accelerates with disease progression.(102,103) Changes in functional connectivity in anterior brain regions seemed to be related to executive dysfunction, whereas changes in more posterior regions may be related to the evolution to dementia.”
Functional connectivity and cognitive decline over 3 years in Parkinson disease
Dubbelink, K. T. E. O., Schoonheim, M. M., Deijen, J. B., Twisk, J. W. R., Barkhof, F., & Berendse, H. W. (2014) · Neurology · doi:10.1212/wnl.0000000000001020 · Cited by 165 · cited 1×
“Changes in functional connectivity in anterior brain regions seemed to be related to executive dysfunction, whereas changes in more posterior regions may be related to the evolution to dementia.(104) Cognitive heterogeneity in PD may be mediated through common genetic variation of several genes including catechol-o-me…”
Automated Neuromelanin Imaging as a Diagnostic Biomarker for Parkinson's Disease
Castellanos, G., Fernández-Seara, M., Lorenzo-Betancor, O., Ortega-Cubero, S., Puigvert, M., Uranga, J., Vidorreta, M., Irigoyen, J., Lorenzo, E., Muñoz-Barrutia, A., et al. (2015) · Movement Disorders · doi:10.1002/mds.26201 · Cited by 164 · cited 1×
“sitive to neuromelanin and show the SNpc as an area of high signal intensity.(93) Reduced size and signal”
Adenosine 2A receptor availability in dyskinetic and nondyskinetic patients with Parkinson disease
Ramlackhansingh, A., Bose, S., Ahmed, I., Turkheimer, F., Pavese, N., & Brooks, D. (2011) · Neurology · doi:10.1212/wnl.0b013e31821ccce4 · Cited by 164
Self-citationChanging the research criteria for the diagnosis of Parkinson's disease: obstacles and opportunities
Berg, D., Lang, A. E., Postuma, R. B., Maetzler, W., Deuschl, G., Gasser, T., Siderowf, A. D., Schapira, A. H. V., Oertel, W. H., Obeso, J. A., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70047-4 · Cited by 164
Self-citationDoherty, K. A., Silveira‐Moriyama, L., Parkkinen, L., Healy, D. G., Farrell, M., Mencacci, N. E., Ahmed, Z., Brett, F. M., Hardy, J., Quinn, N. P., et al. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.172 · Cited by 164
Sequencing analysis of the ITPR1 gene in a pure autosomal dominant spinocerebellar ataxia series
van de Leemput, J., Vrièze, F. W.-D., Rafferty, I., Brás, J., Giunti, P., Fisher, E., Hardy, J. A., Singleton, A., & Houlden, H. (2010) · Movement Disorders · doi:10.1002/mds.22646 · Cited by 163
Lewy pathology is not the first sign of degeneration in vulnerable neurons in Parkinson disease
Milber, J. M., Noorigian, J. V., Morley, J. F., Petrovitch, H., White, L., Ross, G. W., & Duda, J. E. (2012) · Neurology · doi:10.1212/wnl.0b013e318278fe32 · Cited by 163
Self-citationα-Synuclein Suppression by Targeted Small Interfering RNA in the Primate Substantia Nigra
McCormack, A. L., Mak, S. K., Henderson, J. M., Bumcrot, D. A., Farrer, M. J., & Monte, D. A. D. (2010) · PLoS ONE · doi:10.1371/journal.pone.0012122 · Cited by 162 · cited 1×
“More exciting are attempts to disaggregate aggregated synuclein, facilitate its clearance by augmenting autophagy pathways, or using antibodies to prevent its propagation from the periphery to the brain and once in the brain across the neuraxis.(288) Farthest along are vaccines against alphasynuclein as both active an…”
The medical treatment of Parkinson disease from James Parkinson to George Cotzias
Fahn, S. (2014) · Movement Disorders · doi:10.1002/mds.26102 · Cited by 162 · cited 1×
“dopamine in the brain and the second by Oleh Hornykiewicz, who demonstrated that the largest group of dopaminergic neurons are found in the SN with their terminals in the caudate nucleus.(64) The degeneration of the dopaminergic pigmented neurons in the SN is the most consistent neuropathological feature found in all…”
Self-citationSchwarz, S., Abaei, M., Gontu, V., Morgan, P., Bajaj, N., & Auer, D. (2013) · NeuroImage: Clinical · doi:10.1016/j.nicl.2013.10.006 · Cited by 159
Patterns of bursting occurring in thalamic cells during parkinsonian tremor.
Zirh, T., Lenz, F., Reich, S., & Dougherty, P. (1998) · Neuroscience · doi:10.1016/s0306-4522(97)00295-9 · Cited by 155
Goldman, J. G., Stebbins, G. T., Dinh, V., Bernard, B. A., Merkitch, D., deToledo‐Morrell, L., & Goetz, C. G. (2014) · Brain · doi:10.1093/brain/awt360 · Cited by 155
Self-citationRegional patterns of brain tissue loss associated with depression in Parkinson disease
Kostić, V. S., Agosta, F., Petrović, I. N., Galantucci, S., Spica, V., Ječmenica‐Lukić, M., & Filippi, M. (2010) · Neurology · doi:10.1212/wnl.0b013e3181f11c1d · Cited by 153
Lang, A. E. (2011) · Movement Disorders · doi:10.1002/mds.23609 · Cited by 152 · cited 1×
“These motor signs are often preceded by nonmotor manifestations such as olfactory dysfunction in approximately 90%, constipation, REM behavior disorder, and depression/anxiety.(24) As the disease progresses, the clinical picture becomes a composite of levodopa-related motor complications, nondopaminergic motor feature…”
Self-citationClinical implications of delayed orthostatic hypotension
Gibbons, C. H., & Freeman, R. L. (2015) · Neurology · doi:10.1212/wnl.0000000000002030 · Cited by 148
New methods for the assessment of Parkinson's disease (2005 to 2015): A systematic review
Sánchez‐Ferro, Á., Elshehabi, M., Godinho, C., Salkovic, D., Hobert, M. A., Domingos, J., van Uem, J. M., Ferreira, J. J., & Maetzler, W. (2016) · Movement Disorders · doi:10.1002/mds.26723 · Cited by 145 · cited 1×
“applications to noninvasively monitor mobility and motor speed on a large scale.(225) 2.”
Intracranial Self-Stimulation in Man
Bishop, M. P., Elder, S. T., & Heath, R. G. (1963) · Science · doi:10.1126/science.140.3565.394 · Cited by 142 · cited 1×
“DBS had been used since the 1960s for a number of psychiatric and pain disorders.(188) It had been used sporadically to treat movement disorders in the 1970s and 1980s, but it was the introduction of STN DBS by Benabid and Pollak and their team that caused a major impact, only comparable to the one seen when levodopa…”
Marras, C., Lang, A., van de Warrenburg, B. V. D., Sue, C., Tabrizi, S., Bertram, L., Mercimek-Mahmutoglu, S., Ebrahimi-Fakhari, D., Warner, T., Durr, A., et al. (2017) · Movement Disorders · doi:10.1002/mds.27045 · Cited by 141
Self-citationParkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity
Sharman, M. A., Valabrègue, R., Perlbarg, V., Marrakchi‐Kacem, L., Vidailhet, M., Benali, H., Brice, A., & Lehéricy, S. (2012) · Movement Disorders · doi:10.1002/mds.25255 · Cited by 140 · cited 1×
“Reduced connectivity of the SN with the basal ganglia and thalamus were also evidenced in PD patients using tractography-based methods and resting state functional connectivity.(91) In contrast to quantitative mapping, measurements of the morphological changes of the SN seemed unreliable to detect changes related to P…”
Neuropathology of α‐synuclein propagation and braak hypothesis
McCann, H., Cartwright, H., & Halliday, G. M. (2015) · Movement Disorders · doi:10.1002/mds.26421 · Cited by 140 · cited 2×
“The time course of pathological progression is usually very slow, with 50% of patients having limbic LPs on average 13 years following onset, and all having such pathology by 18 years.(75) In patients with Alzheimer pathology (often older at onset), LPs dominate the limbic system and only later may become more widespr…”
Self-citationChemopallidectomy and Chemothalamectomy
Cooper, I. S., & Bravo, G. (1958) · Journal of neurosurgery · doi:10.3171/jns.1958.15.3.0244 · Cited by 139
M itochondrial DNA and primary mitochondrial dysfunction in P arkinson's disease
Giannoccaro, M. P., Morgia, C. L., Rizzo, G., & Carelli, V. (2017) · Movement Disorders · doi:10.1002/mds.26966 · Cited by 137 · cited 1×
“function either by regulating oxidant defenses, mitophagy, or biogenesis.(250) Together, these observations T H E S H A K I N G P A L S Y : P A S T , P R E S E N T A N D F U T U R E”
Muthuraman, M., Heute, U., Arning, K., Anwar, A. R., Elble, R., Deuschl, G., & Raethjen, J. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.01.088 · Cited by 134
Self-citationCorrelation of striatal dopamine transporter imaging with post mortem substantia nigra cell counts
Kraemmer, J., Kovacs, G. G., Perju-Dumbrava, L., Pirker, S., Traub-Weidinger, T., & Pirker, W. (2014) · Movement Disorders · doi:10.1002/mds.25975 · Cited by 132
Trophic Factor Gene Therapy for Parkinson's Disease
Kordower, J. H., & Björklund, A. (2013) · Movement Disorders · doi:10.1002/mds.25344 · Cited by 129 · cited 3×
“Of these, none have received as much attention as members of the glial family of ligands, glial derived neurotrophic factor (GDNF) and neurturin.(275) GDNF was first shown to support the viability of midbrain dopaminergic neurons in culture.”
InfluentialSelf-citationDefining at‐risk populations for Parkinson's disease: Lessons from ongoing studies
Berg, D., MAREK, K. L., Ross, G. W., & Poewe, W. H. (2012) · Movement Disorders · doi:10.1002/mds.24985 · Cited by 128 · cited 1×
“In a population-based study, increased echogenic signal was associated with a 20-fold increased risk of PD (although RBD studies have been more uncertain).(223) Hyperechogenicity is present early in PD and in general more pronounced contralaterally to the clinically more affected side.”
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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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