Relevant bibliographies by topics / Parkinson's disease; Neuroscience

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Parkinson's disease; Neuroscience'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Parkinson's disease; Neuroscience"

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Dauer, William, and Serge Przedborski. "Parkinson's Disease." Neuron 39, no. 6 (September 2003): 889–909. http://dx.doi.org/10.1016/s0896-6273(03)00568-3.

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Allain, Hervé, Danièle Bentué-Ferrer, and Yvette Akwa. "Disease-modifying drugs and Parkinson's disease." Progress in Neurobiology 84, no. 1 (January 2008): 25–39. http://dx.doi.org/10.1016/j.pneurobio.2007.10.003.

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Wider, Christian, Sarah J. Lincoln, Michael G. Heckman, Nancy N. Diehl, Jeremy T. Stone, Kristoffer Haugarvoll, Jan O. Aasly, et al. "Phactr2 and Parkinson's disease." Neuroscience Letters 453, no. 1 (March 2009): 9–11. http://dx.doi.org/10.1016/j.neulet.2009.02.009.

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Agid, Y., and F. Javoy-Agid. "Peptides and Parkinson's disease." Trends in Neurosciences 8 (January 1985): 30–35. http://dx.doi.org/10.1016/0166-2236(85)90012-8.

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William Langston, J. "MPTP and parkinson's disease." Trends in Neurosciences 8 (January 1985): 79–83. http://dx.doi.org/10.1016/0166-2236(85)90031-1.

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Robbins, Trevor W., and Roshan Cools. "Cognitive deficits in Parkinson's disease: A cognitive neuroscience perspective." Movement Disorders 29, no. 5 (April 15, 2014): 597–607. http://dx.doi.org/10.1002/mds.25853.

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Dekker, M. "Mutations in the hemochromatosis gene (HFE), Parkinson's disease and parkinsonism." Neuroscience Letters 348, no. 2 (September 11, 2003): 117–19. http://dx.doi.org/10.1016/s0304-3940(03)00713-4.

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Venhovens, J., J. Meulstee, B. R. Bloem, and W. I. M. Verhagen. "Neurovestibular analysis and falls in Parkinson's disease and atypical parkinsonism." European Journal of Neuroscience 43, no. 12 (May 13, 2016): 1636–46. http://dx.doi.org/10.1111/ejn.13253.

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Vanhauwaert, Roeland, and Patrik Verstreken. "Flies with Parkinson's disease." Experimental Neurology 274 (December 2015): 42–51. http://dx.doi.org/10.1016/j.expneurol.2015.02.020.

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Okai, David. "Neuropsychiatric sequelae of Parkinson's disease: what every clinician needs to know." BJPsych Advances 26, no. 6 (October 30, 2020): 343–45. http://dx.doi.org/10.1192/bja.2020.70.

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SUMMARYJones et al's review of the assessment and management of the neuropsychiatric manifestations of Parkinson's disease serves as a practical guide to clinicians. This commentary outlines some of the underlying neuroscience and psychological sequelae of this range of conditions, offering a takeaway message to the clinician with an interest in Parkinson's neuropsychiatry.
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Dissertations / Theses on the topic "Parkinson's disease; Neuroscience"

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Ikuta, Toshikazu. "fMRI study of grammar, Parkinson's disease and dopaminergic medication." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3337540.

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Thesis (Ph.D.)--Indiana University, Program of Neuroscience and the Dept. of Linguistics, 2008.
Title from PDF t.p. (viewed on Jul 27, 2009). Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6602. Adviser: Laura L. Murray.
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Crocker, Stephen J. "Novel therapeutic strategies for the treatment of Parkinson's disease." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9053.

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Parkinson's disease (PD) is a common neurodegenerative disorder associated with the loss of dopamine neurons located in the substantia nigra pars compacta. Current pharmacological approaches for the treatment of PD are confounded by development of abnormal involuntary movements called dyskinesias, and offer limited long-term utility because they do not stop the disease progression. Accordingly, this thesis addressed two primary issues limiting the present treatments of Parkinson's disease: the molecular basis of dopamine receptor-related dyskinesias, and attenuation of dopamine neuron death. Administration of dopamine receptor agonists to rats with unilateral 6-hydroxydopamine lesions of the nigrostriatal pathway produce changes in the denervated striatum that enable subsequent exposure to dopamine agonists to elicit potentiated circling behaviour, a phenomenon called "priming". Priming is used as a model to study the molecular basis of dyskinesias. Here, I demonstrate that dopamine D1-receptor priming is associated with a profound elevation of the nuclear transcription factor FosB in the denervated striatum. Moreover, intrastriatal delivery of an antisense oligonucleotide to fosB effectively blocked the induction of striatal FosB by dopamine agonist administration and attenuated the circling response elicited by injection of a selective dopamine D1-receptor agonist 3 days later. These findings suggest that dopamine receptor mediated FosB expression in the striatum plays a role in priming. In addition, the results from this study suggest that fosB may be involved the intracellular events which are responsible for the development of dyskinesias following chronic dopamine replacement therapy. The molecular processes which mediate the loss of nigral dopamine neurons in Parkinson's disease are not known. Recently, a novel family of mammalian proteins, called Inhibitor of Apoptosis (IAP) proteins, were cloned and shown to prevent cell death induced by a variety of cytotoxic factors. In two separate studies, I demonstrate that enhanced neuronal expression of two of these IAP proteins, neuronal apoptosis inhibitor protein (NAIP) and X-linked IAP (XIAP), prevents the death of nigral dopamine neurons following exposure to the dopaminergic neurotoxins. In rats, intrastriatal administration of recombinant adenoviruses containing NAIP (Ad.NAIP) was shown to prevent both the cellular and behavioural deficits produced by intrastriatal administration of 6-OHDA when compared to adenovirus control (Ad.lacZ) lesioned animals. Secondly, I describe a novel strain of mice engineered to overexpress XIAP in neurons by using a neuron-specific enolase promoter (NSE-xiap). Moreover, I demonstrate that NSE-xiap mice were profoundly resistant to the deleterious effects of the dopaminergic neurotoxin, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Since administration of MPTP can produce behavioural and neuropathological deficits reminiscent of PD in humans, results from this study suggest that IAP proteins may have utility for the treatment and prevention of cell death in idiopathic PD. Taken together, these studies suggest that neuroprotective strategies based on enhanced neuronal expression of IAP proteins may have novel therapeutic potential for treating neurodegeneration associated with Parkinson's disease.
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Biswas, Amitava. "Perioral sensorimotor integration in Parkinson's disease." [Bloomington, Ind.] : Indiana University, 2005. http://wwwlib.umi.com/dissertations/fullcit/3183913.

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Alexopoulou, Zoi. "The study of the deubiquitinase USP8 in Parkinson's disease pathogenesis." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:47c2941b-5232-4bd0-92fa-e59aac16af7c.

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Parkinson's disease is the second commonest neurodegenerative disease currently treated symptomatically. It is a multifactorial disease involving mechanisms ranging from protein aggregation to mitochondrial dysfunction, oxidative stress and dopamine dysregulation. The levels of α-synuclein have been causatively linked to the development and progression of Parkinson's disease. Therefore α-synuclein lowering strategies are valid approaches in Parkinson's disease. Neuropathologically, Lewy Bodies in the vulnerable substantia nigra of Parkinson's disease patients are less ubiquitinated and specifically less K-63 ubiquitinated than Lewy bodies in the cortex, suggesting differential activation or regulation of ubiquitin interactors. A targeted screen for such interactors revealed that the Deubiquitinating enzyme Usp8 is upregulated in the substantia nigra of Parkinson's disease brains and is inversely correlated with the degree of total and K-63 ubiquitination. Using genetic knockdown and overexpression techniques, Usp8 was found to colocalize and directly interact with α-synuclein. It was found to de-ubiquitinate α-synuclein and increase its half-life. Its knockdown increased the total and K-63 α-synuclein ubiquitination and decreased its levels by 35% at least partly by increasing its degradation via the lysosome. In vivo in the Drosophila melanogaster, Usp8 knockdown demonstrated protection against α-synuclein toxicity. It rescued in a specific manner the rough eye phenotype, the age-dependent locomotive defect and the loss of dopaminergic neurons caused by the expression of α-synuclein. Specific and effective pharmacological Usp8 inhibition also has the potential to lower α-synuclein levels. Collectively, the evidence produced in my thesis suggests that Usp8 could be a potential target for the future disease-modifying therapies in Parkinson's disease.
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Little, Simon. "Adaptive deep brain stimulation for Parkinson's disease : closed loop stimulation for Parkinson's." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5b76616a-7d5e-424e-9c66-5d48b19cae1c.

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Our understanding of the pathophysiology Parkinson’s disease has transformed over the last decade as we have come to appreciate the importance of changes in neuronal firing pattern that occur within the motor network in the dopamine deficient state. These changes in firing pattern, particularly increased synchrony result in oscillations that can be recorded as local field potentials. This thesis concerns itself with the study of beta oscillations which are characteristic of Parkinson’s disease. Firstly, I investigate whether beta oscillations play a pathophysiological role in Parkinson’s disease or whether they are purely epiphenomenal by augmenting beta with low frequency deep brain stimulation. In this study I show that rigidity is increased by ~25% with low frequency stimulation providing significant further evidence for a patho-physiological role of beta in Parkinson’s disease. Next I investigate whether beta oscillations correlate with Parkinsonian severity at rest and could therefore potentially be used as a biomarker of clinical state. I demonstrate that the variability of beta amplitude recorded from the subthalamic nucleus strongly correlates with symptom severity at rest and also in response to levodopa administration. I then use beta amplitude as a biomarker for a trial of adaptive deep brain stimulation in Parkinson’s disease. I show that by using beta amplitude to control stimulation, time on stimulation is reduced by >50% but despite this, clinical outcome is improved by 25% relative to conventional continuous high frequency stimulation. Finally, I investigate the bilateral subcortical beta network and its response to levodopa. I report statistically significant bilateral functional connectivity in the beta range which is driven by phase locking and modulated by levodopa in the low beta range with implications for bilateral adaptive deep brain stimulation. These findings further our understanding of the pathophysiological role of beta oscillations in Parkinson’s disease and provide new avenues for treatment development.
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Marshall, Victoria Louise. "Clinical and functional imaging correlates in Parkinson's disease." Thesis, University of Glasgow, 2006. http://theses.gla.ac.uk/7012/.

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Parkinson's disease (PD) is misdiagnosed throughout its disease course for conditions such as essential tremor, drug-induced parkinsonism, vascular pseudo-parkinsonism, Alzheimer's disease and other degenerative parkinsonian diseases. This thesis aims to verify the accuracy of dopaminergic imaging in early and uncertain parkinsonian/tremor disorders through 3 studies. The first is a prospective United Kingdom multicentre assessment of [1231] FP-CIT SPECT use in 190 patients in pre-defined diagnostic categories and with particular focus on clinical features to assess the influence of imaging in routine practice. The second is a 2 year follow-up study of 150 consecutive patients with normal SPECT, with specific attention to clinical progression and antiparkinson medication use, and includes focus on a subgroup who fulfilled PD criteria where successful antiparkinson medication withdrawal was achieved. The third is a multicentre prospective European study of the accuracy of [1231] FP-CIT SPECT in 99 patients that included serial clinical and imaging assessments. Notably, when initial diagnosis/scan mismatch cases occurred, and with awareness of the scan result, the clinician invariably changed the diagnosis in line with the scan result which confirms the considerable influence of imaging on the practising clinician. Parkinson's disease is clinically overdiagnosed early in its disease course, whereas imaging is more specific, in the vast majority of cases with normal dopaminergic imaging, there was no evidence of clinical or imaging progression which would be in keeping with degenerative parkinsonism.
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Kabbach, Ghassan. "Interactions of LRRK2 in a Drosophila melanogaster model of Parkinson's disease." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28820.

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Parkinson's disease is the most common movement disorder. A complex neurodegenerative disease, its cause and progressive nature are of unknown roots, making a final cure currently unattainable. Recently, mutations in LRRK2 have been deemed the most common cause of both familial and sporadic forms of Parkinson's disease. Itself a mysterious protein, it harbors pathogenic mutations in all of its complex functional domains. Here, we present a Drosophila melanogaster model of LRRK2 by creating four different human LRRK2 transgenic flies. Wild type LRRK2, and LRRK2 mutants I1122V, Y1699C, and I2020T have each demonstrated Dopamine neuron loss, complex behavioral and life span alterations, and a complex eye phenotype. Lastly, we have used the eye phenotype to conduct both a biased screen against recessive Parkinson's disease genes, and an unbiased screen against the Drosophila genome.
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Acosta, Glen Howel G. "Susceptibility of parkinson's disease following mild blast traumatic brain injury." Thesis, Purdue University, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1571943.

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Blast injury-induced neurotrauma (BINT) is steadily increasing in prevalence due to escalated terror activity and constitutes the signature injury associated with current military conflicts. BINT produces significant neurological deficiencies and there is a growing concern that the injury may produce long-term consequences that affect the resilience and the performance of soldiers. One of the potential consequences is an increased susceptibility to Parkinson's disease (PD). A vital goal aimed at curtailing the post-deployment long-term consequences of blast injury-induced neurotrauma is to further our knowledge of pathogenic mechanisms responsible for the escalation of post injury diseases. The purpose of this project is to investigate the molecular mechanism underlying the susceptibility of PD in post-blast rats. We have identified acrolein, a highly reactive aldehyde that persists days to weeks following brain-injury and perpetuates oxidative insult, as a potential therapeutic target to curtail chemically mediated damage, a common feature of BINT and PD. Our hypothesis is that acrolein is a key pathological factor linking BINT and the development of PD in our rat model.

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Song, Linyang 1978. "The role of astroglial HO-1 in the pathogenesis of Parkinson's disease /." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98803.

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The mechanisms responsible for the progressive loss of dopaminergic neurons and pathological iron deposition in the substania nigra pars compacta of patients with Parkinson disease (PD) remain incompletely understood. Heme oxygenase-1 (HO-1), the rate-limiting enzyme in the degradation of heme to biliverdin, carbon monoxide, and ferrous iron, is up-regulated in affected PD astroglia and may contribute to aberrant mitochondrial iron sequestration in these cells. To determine whether glial HO-1 hyperexpression is inimical to nearby neuronal constituents, we co-cultured dopaminergic PC12 cells atop monolayers of human (h) HO-1 transfected, sham-transfected or non-transfected primary rat astroglia. We observed that PC12 cells grown atop hHO-1 transfected astrocytes, but not the astroglia themselves, were significantly more vulnerable to dopamine (1muM) + H2O2 (1muM)-induced death (measured by nuclear ethidium monoazide bromide staining and anti-TH immunofluorescence microscopy) relative to control preparations. In the experimental group, PC12 cell death was significantly attenuated by the administration of the HO inhibitor, SnMP (1.5muM), the antioxidant, ascorbate (200muM), or the iron chelators, deferoxamine (400muM) and phenanthroline (100muM). Exposure to conditioned media derived from HO-1 transfected astrocytes also augmented PC12 cell killing in response to dopamine (1muM) + H2O2 (1muM) relative to control media. In PD patients, over-expression of HO-1 in nigral astroglia and attendant iron liberation may facilitate the bioactivation of dopamine to neurotoxic free radical intermediates and predispose nearby neuronal constituents to oxidative damage.
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Malek, Naveed. "Variation in Parkinson's disease : age, gender, genotype and phenotype correlations in early onset disease." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5602/.

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There is a wide variation in the phenotypic expression, progression rates, therapy response and complications in Parkinson’s disease (PD). The primary research objective in this thesis was to analyse the variation in the 4 domains of phenotypic expression i.e. motor, non-motor, cognitive, and quality of life in a subset of early onset Parkinson’s disease (EOPD) patients from the PRoBaND study, in the United Kingdom. The secondary objective was to explore the factors responsible for this variation or heterogeneity in the clinical characteristics. Linking genotypes with phenotypes, besides evaluating environmental risk factors and iatrogenic influences, represents one mechanism of understanding this variation in the phenotypic expression of PD. We found subtle but significant variation across all domains of symptoms examined in this thesis by classifying patients into groups according to motor subtype, gender, age at diagnosis and heritability of the parkinsonian trait, despite statistically insignificant differences in risk factors such as head trauma, exposure to pesticides (including herbicides, insecticides, fungicides and fumigants), heavy metals, caffeine and a past history of oophorectomy (in females) with the exception of smoking (p=0.046) and exposure to solvents, which were more common in males compared to females (p<0.001). There were differences in the prevalence of motor symptoms such as balance problems being more prevalent in the postural instability gait difficulty (PIGD) subtype compared to the tremor dominant PD (TDPD) and ‘Mixed’ motor subtypes both subjectively (p<0.001) and objectively (p<0.001). Other axial problems such as speech difficulties and freezing were also more prevalent in those with the PIGD phenotype compared to the other motor subtypes both subjectively (p=0.004, p<0.001) and objectively (p=0.002, p<0.001). There was also variation in the prevalence of motor complications such as dyskinesia (p<0.001) and dystonia (p=0.020), being more prevalent in the PIGD subtype compared to other motor subtypes. 8 The prevalence of certain non-motor symptoms such as pain (p=0.022) and features of gastrointestinal dysfunction e.g. prandial bloating (p=0.024) and constipation (p=0.022) were more commonly reported by females compared to males. There were also differences in the prevalence of cognitive impairment (p=0.049) and neurobehavioural characteristics such as anxiety (p=0.002) and depression (p=0.006), after the diagnosis of PD, being more prevalent in PIGD compared to other motor subtypes. Finally, these differences contributed to the variation in the independence of activities of daily living scores which were lower in those with the PIGD phenotype compared to other motor subtypes (p<0.001). There were some differences in exposure to environmental risk factors for PD but not sufficient to explain all the variation. Iatrogenic influences from drugs contributed in part to the phenotypic variation. 10% of the cases in the EOPD cohort tested positive for mutations in one of three genes screened i.e. LRRK2, GBA and Parkin; their DNA remains banked and there is scope to test these cases for mutations in other genes, relevant to PD, in the future. There were too small numbers of cases in each subgroup to draw definite conclusions about the exact influence of genes on the overall phenotypic variation but differences between Parkin mutation carriers and gene test negative ‘controls’ such as early age of onset and long disease duration were obvious. PRoBaND is linked to other similar research studies in the UK, with the stated aim of sharing datasets, in the hope that larger numbers of patients and their DNA samples will increase the power, in statistical terms, to test hypotheses about the role of genetic markers in influencing the course and expression of symptoms. Our current understanding of PD as a complex trait suggests both genetic and environmental influences (including iatrogenic factors if patients are treated) play a role in the phenotypic expression of this condition. A lot more remains to be explored to improve our understanding of the finer details and molecular mechanisms underlying the variation in this disease.
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Books on the topic "Parkinson's disease; Neuroscience"

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Recent advances in Parkinson's disease. Amsterdam: Elsevier, 2010.

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Pieter, Voorn, Berendse Henk W, Mulder Antonius B, Cools Alexander Rudolf 1941-, and SpringerLink (Online service), eds. The Basal Ganglia IX. New York, NY: Springer-Verlag New York, 2009.

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Hirosaki International Forum of Medical Science (6th 2002 Hirosaki-shi, Japan). Advances in brain research: Cerebrovascular disorders and neurodegeneration : proceedings of the 6th Hirosaki International Forum of Medical Science, held in Hirosaki, Japan, between 15 and 16 October 2002. Edited by Satoh Kei, Suzuki Shigeharu M. D, and Matsunaga Muneo. Amsterdam: Elsevier, 2003.

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Neuroscience of Parkinson's Disease. Elsevier Science & Technology, 2020.

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Preedy, Victor R., and Colin R. Martin. Neuroscience of Parkinson's Disease. Elsevier Science & Technology Books, 2020.

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Tolosa, Eduardo, and Joseph J. Jankovic. Parkinson's Disease & Movement Disorders. 4th ed. Lippincott Williams & Wilkins, 2002.

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Joseph, Jankovic, and Tolosa Eduardo, eds. Parkinson's disease and movement disorders. 4th ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2002.

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(Editor), C. W. Olanow, Peter Jenner (Editor), and Moussa Youdim (Editor), eds. Neurodegeneration and Neuroprotection in Parkinson's Disease (Neuroscience Perspectives). Academic Press, 1996.

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Preedy, Victor R., and Colin R. Martin. Diagnosis and Management in Parkinson's Disease: The Neuroscience of Parkinson's, Volume 1. Elsevier Science & Technology Books, 2020.

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Preedy, Victor R., and Colin R. Martin. Diagnosis and Management in Parkinson's Disease: The Neuroscience of Parkinson's, Volume 1. Elsevier Science & Technology, 2020.

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Book chapters on the topic "Parkinson's disease; Neuroscience"

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Elkis-Abuhoff, Deborah, and Morgan Gaydos. "Medical Art Therapy Applied to the Trauma Experienced by those Diagnosed with Parkinson's Disease." In Art Therapy, Trauma, and Neuroscience, 195–210. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781003196242-9.

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Double, Kay, and John Finberg. "Parkinson’s Disease." In Neuroscience in the 21st Century, 2903–21. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1997-6_112.

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Double, Kay, and John Finberg. "Parkinson’s Disease." In Neuroscience in the 21st Century, 3843–61. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3474-4_112.

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Bratt-Leal, Andrés M., and Jeanne F. Loring. "Stem Cells for Parkinson’s Disease." In Translational Neuroscience, 187–201. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7654-3_11.

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Ceballos-Picot, Irène. "Oxidative Stress in Parkinson’s Disease." In Neuroscience Intelligence Unit, 175–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-22516-5_8.

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Kaplitt, Michael G., and Matthew J. During. "GAD Gene Therapy for Parkinson’s Disease." In Translational Neuroscience, 89–98. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7654-3_5.

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Beuter, Anne. "Parkinson’s Disease: Deep Brain Stimulation." In Encyclopedia of Computational Neuroscience, 2213–21. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_510.

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Müller, F., and G. E. Stelmach. "Scaling Problems in Parkinson’s Disease." In Tutorials in Motor Neuroscience, 161–74. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3626-6_14.

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Beuter, Anne. "Parkinson’s Disease: Deep Brain Stimulation." In Encyclopedia of Computational Neuroscience, 1–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_510-2.

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Lavano, Angelo, and Anne Beuter. "Parkinson’s Disease: Deep Brain Stimulation." In Encyclopedia of Computational Neuroscience, 1–12. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-7320-6_510-3.

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Conference papers on the topic "Parkinson's disease; Neuroscience"

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Chong, Raymond, Chandramohan Wakade, and Eric Bradley. "Plasma Cytokines and Sleep Quality in Parkinson's Disease." In Annual International Conference on Neuroscience and Neurobiology Research. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2345-7813_cnn14.09.

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Alessenko, Alice, Viktor Blokhin, Sergei Sokolov, Olga Maloshitskaya, Uliana Gutner, Maria Shupik, and Michael Ugryumov. "ROLE OF SPHINGOLIPIDS IN THE PATHOGENESIS OF PARKINSON'S DISEASE." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m909.sudak.ns2020-16/59.

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Chigaleychik, Larisa, Elena Teslenko, and Vsevolod Poleschuk. "STABILOMETRIC INDICATORS IN THE EARLY STAGES OF PARKINSON'S DISEASE." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2401.sudak.ns2021-17/423-424.

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Grachova, Elizaveta, Anastsia Kudrevatykh, Irina Miliukhina, Tatiana Novikova, Timofey Sergeev, and Nikolay Suvorov. "AUTONOMIC DISORDERS IN PARKINSON'S DISEASE AND METHODS OF THEIR CORRECTION." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1005.sudak.ns2020-16/161.

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Rajendran, Arathi, Anuja Thankamani, Nishamol Nirmala, Bipin Nair, and Shyam Diwakar. "Computational neuroscience of substantia nigra circuit and dopamine modulation during parkinson's disease." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8125892.

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Khidiyatova, Irina, Gulnara Akhmadeeva, Irina Gilyazova, Anastasiya Petrova, Azamat Baitimerov, Rim Magzhanov, and Elza Khusnutdinova. "THE ROLE OF MONOAMINE METABOLISM SYSTEM GENES IN NEUROPSYCHOLOGICAL MANIFESTATIONS OF PARKINSON'S DISEASE." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1317.sudak.ns2020-16/494-495.

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Danilova, Nina, and Elena Strabykina. "IN THE PATIENTS WITH PARKINSON'S DISEASE REVEALED INCREASED ALPHA RHYTHM, WHICH EXCEEDS THE NORM." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m376.sudak.ns2019-15/158-159.

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Ryabchikova, Nataliya, Elena Damjanovic, Larisa Chigaleychik, and Boris Baziyan. "SACCAD EYES MOVEMENTS UNDER PROGNOSTIC ACTIVITY IN PATIENTS WITH EARLY STAGES OF PARKINSON'S DISEASE." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m538.sudak.ns2019-15/356-358.

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Bazyan, Ara. "COMMON PROCESSES OF DEVELOPMENT OF VARIOUS PATHOLOGIES: DRUG ADDICTION, ABSENCE EPILEPSY, PARKINSON'S DISEASE, RADIATION DISORDERS." In XIV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2018. http://dx.doi.org/10.29003/m174.sudak.ns2018-14/88.

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Bondarchuk, Vladimir. "COMPLEX METHOD OF NEUROLOGY, REFLEXOLOGY AND MANUAL THERAPY IN REHABILITATION OF PATIENTS WITH PARKINSON'S DISEASE." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2063.sudak.ns2021-17/86-87.

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