Relevant bibliographies by topics / Parkinson's disease; Huntington's disease

Contents

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

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

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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

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Teräväinen, H., M. Hietanen, J. Stoessl, and D. B. Calne. "Dementia in Movement Disorders." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (November 1986): 546–58. http://dx.doi.org/10.1017/s031716710003729x.

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Abstract:Of all the movement disorders, Huntington's disease has been most consistently associated with dementia, while it is only over the last decade that intellectual and cognitive decline have been recognized as common features of Parkinson's disease. It is now known that the pathology in these two conditions reflects differential involvement of the striatum. The Huntington lesion is primarily in the caudate, while the Parkinson lesion preferentially affects the putamen. Both conditions have more diffuse pathology, and dementia may also occur in a wide range of other extrapyramidal diseases, such as progressive supranuclear palsy, the parkinsonism-dementia complex of Guam, and certain spinocerebellar degenerations. Clinicopathological correlations will be reviewed in these disorders of primarily subcortical pathology, and comparisons will be made with Alzheimer's disease, a disorder of predominantly cortical pathology.
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Hague, S. M. "Neurodegenerative disorders: Parkinson's disease and Huntington's disease." Journal of Neurology, Neurosurgery & Psychiatry 76, no. 8 (August 1, 2005): 1058–63. http://dx.doi.org/10.1136/jnnp.2004.060186.

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Hanes, K. R., D. G. Andrewes, and C. Pantelis. "Dysfluency in Huntington's disease, Parkinson's disease and schizophrenia." Applied Neuropsychology 2, no. 1 (February 1995): 29–34. http://dx.doi.org/10.1207/s15324826an0201_5.

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O’Keeffe, Gráinne C., Andrew W. Michell, and Roger A. Barker. "Biomarkers in Huntington's and Parkinson's Disease." Annals of the New York Academy of Sciences 1180, no. 1 (October 2009): 97–110. http://dx.doi.org/10.1111/j.1749-6632.2009.04943.x.

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Ramig, Lorraine A., Ingo R. Titze, Ronald C. Scherer, and Steven P. Ringel. "Acoustic Analysis of Voices of Patients with Neurologic Disease: Rationale and Preliminary Data." Annals of Otology, Rhinology & Laryngology 97, no. 2 (March 1988): 164–72. http://dx.doi.org/10.1177/000348948809700214.

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This paper presents a rationale for acoustic analysis of voices of neurologically diseased patients, and reports preliminary data from patients with myotonic dystrophy, Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as from individuals at risk for Huntington's disease. Noninvasive acoustic analysis may be of clinical value to the otolaryngologist, neurologist, and speech pathologist for early and differential diagnosis and for documenting disease progression in these various neurologic disorders.
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Dimovski, E. B., J. C. Stout, S. A. Wylie, and E. R. Siemers. "Spatial cognitive shifting in huntington's disease and parkinson's disease." Archives of Clinical Neuropsychology 14, no. 1 (January 1, 1999): 126. http://dx.doi.org/10.1093/arclin/14.1.126.

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Davies, Katherine M., Julian F. B. Mercer, Nicholas Chen, and Kay L. Double. "Copper dyshomoeostasis in Parkinson's disease: implications for pathogenesis and indications for novel therapeutics." Clinical Science 130, no. 8 (March 8, 2016): 565–74. http://dx.doi.org/10.1042/cs20150153.

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Copper is a biometal essential for normal brain development and function, thus copper deficiency or excess results in central nervous system disease. Well-characterized disorders of disrupted copper homoeostasis with neuronal degeneration include Menkes disease and Wilson's disease but a large body of evidence also implicates disrupted copper pathways in other neurodegenerative disorders, including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis, Huntington's disease and prion diseases. In this short review we critically evaluate the data regarding changes in systemic and brain copper levels in Parkinson's disease, where alterations in brain copper are associated with regional neuronal cell death and disease pathology. We review copper regulating mechanisms in the human brain and the effects of dysfunction within these systems. We then examine the evidence for a role for copper in pathogenic processes in Parkinson's disease and consider reports of diverse copper-modulating strategies in in vitro and in vivo models of this disorder. Copper-modulating therapies are currently advancing through clinical trials for Alzheimer's and Huntington's disease and may also hold promise as disease modifying agents in Parkinson's disease.
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Fink, J. Stephen, James M. Schumacher, Samuel L. Ellias, E. Prather Palmer, Marie Saint-Hilaire, Kathleen Shannon, Richard Penn, et al. "Porcine Xenografts in Parkinson's Disease and Huntington's Disease Patients: Preliminary Results." Cell Transplantation 9, no. 2 (March 2000): 273–78. http://dx.doi.org/10.1177/096368970000900212.

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The observation that fetal neurons are able to survive and function when transplanted into the adult brain fostered the development of cellular therapy as a promising approach to achieve neuronal replacement for treatment of diseases of the adult central nervous system. This approach has been demonstrated to be efficacious in patients with Parkinson's disease after transplantation of human fetal neurons. The use of human fetal tissue is limited by ethical, infectious, regulatory, and practical concerns. Other mammalian fetal neural tissue could serve as an alternative cell source. Pigs are a reasonable source of fetal neuronal tissue because of their brain size, large litters, and the extensive experience in rearing them in captivity under controlled conditions. In Phase I studies porcine fetal neural cells grafted unilaterally into Parkinson's disease (PD) and Huntington's disease (HD) patients are being evaluated for safety and efficacy. Clinical improvement of 19% has been observed in the Unified Parkinson's Disease Rating Scale “off” state scores in 10 PD patients assessed 12 months after unilateral striatal transplantation of 12 million fetal porcine ventral mesencephalic (VM) cells. Several patients have improved more than 30%. In a single autopsied PD patient some porcine fetal VM cells were observed to survive 7 months after transplantation. Twelve HD patients have shown a favorable safety profile and no change in total functional capacity score 1 year after unilateral striatal placement of up to 24 million fetal porcine striatal cells. Xenotransplantation of fetal porcine neurons is a promising approach to delivery of healthy neurons to the CNS. The major challenges to the successful use of xenogeneic fetal neuronal cells in neurodegenerative diseases appear to be minimizing immune-mediated rejection, management of the risk of xenotic (cross-species) infections, and the accurate assessment of clinical outcome of diseases that are slowly progressive.
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Boecker, H., A. Ceballos-Baumann, P. Bartenstein, A. Weindl, H. R. Siebner, T. Fassbender, F. Munz, M. Schwaiger, and B. Conrad. "Sensory processing in Parkinson's and Huntington's disease." Brain 122, no. 9 (September 1999): 1651–65. http://dx.doi.org/10.1093/brain/122.9.1651.

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Ludlow, Christy L., Nadine P. Connor, and Celia J. Bassich. "Speech timing in Parkinson's and Huntington's disease." Brain and Language 32, no. 2 (November 1987): 195–214. http://dx.doi.org/10.1016/0093-934x(87)90124-6.

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Dissertations / Theses on the topic "Parkinson's disease; Huntington's disease"

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Gonsalves, Crystal. "Bimanual coordination in Huntington's disease and Parkinson's disease." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27588.

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Special populations that suffer from Parkinson's disease (PD) and Huntington's disease (HD) display poorer performance in movement and bimanual coordination tasks. Both PD and HD are basal ganglia disorders with neuropathology distinct from one another. The production of internally guided movements is disrupted in PD and HD, therefore utilization of the external pathway may be able to stabilize movements for these groups. The current study examines the effect of auditory cueing for these two populations in timing performance. A total of 10 PD patients, 10 healthy controls (matched for age and gender) and 2 HD patients were examined on a repetitive bimanual finger tapping task. PD patients and healthy controls were asked to perform finger tapping at two different frequencies (1.0 Hz, 2.0 Hz) and two movement types (in-phase, anti-phase). Additionally half of the trials were performed with an external cue (metronome beat), while the other half were not (cue was turned off after 10 metronome heats). Results showed that PD patients were able to effectively use the cue to facilitate bimanual coordination as it was shown that absolute mean timing errors were decreased during the cue trials. PD patients were able to perform both movement types although the more complex mirror asymmetrical anti-phase trials were more difficult to perform. HD patients were not able to achieve the designated fast and slow frequencies that PD and healthy controls performed. The HD patients' movement was highly variable due to tremors and involuntary tics experienced by the patients. Through the examination of raw trajectories and polar plots of phase differences it was concluded that the external cue did not seem to stabilize bimanual coordination for the HD patients.
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Gu, Mei. "Mitochondrial function in Parkinson's disease and other neurodegenerative diseases." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322371.

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Underwood, Mandy. "Pain and psychological factors in Huntington's disease and Parkinson's disease." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/33297.

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Background: Chronic pain is a common aspect of many neurological conditions and often causes psychological distress. A scoping literature search revealed research was lacking in the area of Huntington’s disease (HD) and pain, therefore the empirical work focused on providing data on prevalence of pain and psychological predictors of pain in HD. There was insufficient research on HD and pain to form the basis of a review, however there was a body of literature on Parkinson’s disease (PD). The review focused on the relationship between pain and depression in people with PD. A critical appraisal of the experience of conducting the review and empirical work formed the final part of the thesis. Literature review: Fourteen articles were identified and reviewed in depth. Half of the studies, representing approximately three quarters of the participants in total, found a significant relationship between pain and depression in PD, with increased pain associated with increased depression. There was reasonable evidence to support an association between the severity of depression and the severity of pain in people with PD, although further research was recommended. Empirical report: A data-mining study was undertaken using data from 1474 participants of the European Huntington’s Disease Network (EHDN) REGISTRY study to examine the prevalence of pain in HD and to identify, using ordinal regression analysis, which psychological factors predicted severity of pain in people with HD. The prevalence of pain in HD was found to be 41%. Pain severity in HD was predicted by anxiety, depression and irritability. Caregivers and health professionals should consider the possibility that people with HD might be experiencing pain, particularly if there are signs of anxiety, depression or irritability. Recommendations were made for further research and limitations were discussed. Critical appraisal: The research process, methodology and main learning points were considered.
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Orth, Michael. "Molecular study of cell culture models of Parkinson's disease and Huntington's disease." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445761/.

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The discovery of the genetic basis of neurodegenerative disorders has enabled the generation of models to study their pathogenesis. In part one, human embryonic kidney cells with inducible expression of wild-type or mutant G209A cc-synuclein modelled increased a-synuclein expression and a familial form of Parkinson's disease, respectively. Both wild-type and mutant a- synuclein were localised to vesicles, some of which were catecholaminergic. Over- expression of wild-type or mutant (G209A) a-synuclein alone did not reduce cell viability, cause oxidative stress or impair mitochondrial function. However, mutant a- synuclein expression enhanced the susceptibility to dopamine toxicity causing increased oxidative stress and cell death. This effect was similar to that of reserpine, an inhibitor of vesicular monoamine uptake, in controls. These results suggest that a-synuclein may play a role in dopamine compartmentalisation. Loss of function conferred by the G209A mutation could therefore increase cytoplasmic dopamine concentrations with subsequent cell damage or death. In part two, myoblast cell lines were established, and characterised, from the R6/2 mouse model of Huntington's disease (HD). Mutant N-terminal huntingtin transgene over-expression was associated with significantly greater numbers of myotubes suggesting a role of huntingtin in muscle differentiation. In long-term culture, differentiated R6/2 myotubes, but not controls, formed nuclear huntingtin inclusions. Inclusion number depended upon culture medium conditions suggesting that environmental factors might be relevant. This model of HD in non-neuronal post mitotic cells may be useful to study the pathophysiology of, and possibly the effect of therapeutics on, huntingtin aggregate formation. The third part examined the suggestion that codon 129 homozygosity of the prion protein (PrP) gene may predispose to sporadic inclusion body myositis (sIBM). Codon 129 zygosity in 41 sIBM muscle biopsies was not significantly different to results published in population studies in several Western countries suggesting sIBM is not linked to homozygosity at codon 129 of the PrP gene.
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Pretsell, Douglas Ogilvy. "The role of the dorsal striatum in the control of reaction time performance." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261652.

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Keenan, Siobhan Elizabeth. "Language and the basal ganglia : insights from Parkinson's and Huntington's disease." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615882.

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Johnson, Katherine A. (Katherine Anne) 1973. "Movement preparation and execution in Huntington's and Parkinson's diseases." Monash University, Dept. of Psychology, 2001. http://arrow.monash.edu.au/hdl/1959.1/9176.

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Antoniades, Chrystalina Andrea. "The development and optimization of biomarkers for Huntington's and Parkinson's disorders." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609075.

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Ferreira, Danilo Avelar Sampaio. "Avaliação do efeito protetor do beta-cariofileno em modelos celulares de doenças neurodegenerativas." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-17042015-093013/.

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As doenças neurodegenerativas (DN) estão entre as principais causas de mortalidade e morbidade nos países ocidentais. Não há ainda um tratamento definitivo para estas neuropatias, mas estudos têm indicado mecanismos comuns de toxicidade que incluem disfunção mitocondrial, estresse oxidativo, apoptose e neuroinflamação. Adicionalmente, o efeito benéfico da neuroplasticidade induzida por fatores neurotróficos no retardamento ou inibição do processo neurodegenerativo também tem sido sugerido por muitos estudos. O beta-cariofileno é um sesquiterpeno bi-cíclico encontrado no óleo essencial de algumas plantas, e que possui efeito anti-inflamatório e antioxidante. Assim, este composto possui características e é capaz de induzir efeitos que o tornam um potencial candidato ao tratamento/prevenção dos processos envolvidos na neurodegeneração. Apesar disso, pouco se sabe sobre os efeitos e os mecanismos de ação do beta-cariofileno no processo de degeneração neuronal. Então, neste estudo, avaliou-se o efeito do beta-cariofileno em modelos celulares (PC 12) de neurotoxicidade que mimetizam in vitro os mecanismos moleculares envolvidos nas doenças de Parkinson, Huntington e Alzheimer, os quais, para efeitos práticos, denominaremos de \"modelos celulares de Parkinson, Huntington e Alzheimer\". Estes modelos são induzidos experimentalmente pela neurotoxina dopaminérgica iodeto de 1-metil 4-fenil piridina (MPP+), pela neurotoxina mitocondrial ácido 3-nitropropiônico (3NP) e pelo peptídeo neurotóxico B-amiloide (AB42), respectivamente. O beta-cariofileno apresentou efeitos benéficos nestes três modelos de neurotoxicidade, e adicionalmente induziu neuritogênese e a expressão de proteínas neurotípicas no modelo neuronal. Este é o primeiro estudo a demonstrar tais efeitos do beta-cariofileno.
Neurodegenerative diseases (ND) are among the leading causes of mortality and morbidity in Western countries. There is not a definitive treatment for these neuropathies, but studies have indicated common mechanisms of toxicity that include mitochondrial dysfunction, oxidative stress, neuroinflammation and apoptosis. Additionally, the beneficial effect of the neuroplasticity induced by neurotrophic factors on the retardation or inhibition of neurodegeneration has also been suggested by several studies. Beta-caryophyllene is a bicyclic sesquiterpene found in essential oils of some plants, and possesses anti-inflammatory and antioxidant effects. Thus, this compound has characteristics and is capable of inducing effects that make it a potential candidate for treatment / prevention of the processes involved in neurodegeneration. Despite this, little is known about the effects and mechanisms of action of beta-caryophyllene in the neuronal degeneration process. Then, this study evaluated the effect of beta-caryophyllene in cellular models of neurotoxicity (PC 12) that mimic in vitro the molecular mechanisms involved in Parkinson\'s, Huntington\'s and Alzheimer\'s diseases, which, for practical purposes, we will denominate \"Cellular models of Parkinson\'s, Huntington\'s and Alzheimer\'s diseases.\" These models are experimentally induced by the dopaminergic neurotoxin 1-methyl iodide, 4-phenyl pyridine (MPP+), by the mitochondrial neurotoxin 3-nitropropionic acid (3NP) and the neurotoxic peptide B-amyloid (AB42), respectively. Beta-caryophyllene showed beneficial effects on these three models of neurotoxicity, and additionally induced neuritogenesis and the expression of neurotypic proteins in the neuronal model. This is the first study to demonstrate such effects of beta-caryophyllene.
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Gobbel, John Randall. "The role of the neostriatum in the execution of action sequences /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9808981.

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Books on the topic "Parkinson's disease; Huntington's disease"

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Nguyen, Hoa Huu Phuc, and M. Angela Cenci, eds. Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46344-4.

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F, Emerich Dwaine, Dean Reginald L, and Sanberg Paul R, eds. Central nervous system diseases: Innovative animal models from lab to clinic. Totowa, N.J: Humana Press, 2000.

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Association, Huntington's Disease. Huntington's Disease. London (108 Battersea High Street, London SW11 3HP): Huntington's Disease Association, 1994.

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Naff, Clay Farris. Huntington's disease. Detroit: Greenhaven Press, 2012.

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Huntington's disease. New York: Chelsea House, 2009.

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Huntington's disease. New York: The Rosen Pub. Group, 2007.

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Huntington's disease. New York: Cavendish Square Publishing, 2016.

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P, Hammerstad John, and Gancher Stephen T, eds. Parkinson's disease. London: Edward Arnold, 1992.

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Parkinson's disease. Mankato, Minn: Creative Education, 2012.

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Landau, Elaine. Parkinson's disease. New York: F. Watts, 1999.

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

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Biglan, Kevin M., and Ira Shoulson. "Huntington's Disease." In Therapeutics of Parkinson's Disease and Other Movement Disorders, 293–315. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470713990.ch19.

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De Souza, Rebecca A. G., and Blair R. Leavitt. "Neurobiology of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 81–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_353.

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Ghosh, Rhia, and Sarah J. Tabrizi. "Clinical Aspects of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 3–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_238.

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Mrzljak, Ladislav, and Ignacio Munoz-Sanjuan. "Therapeutic Strategies for Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 161–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_250.

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Brooks, Simon P., and Stephen B. Dunnett. "Mouse Models of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 101–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_256.

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Waldvogel, Henry J., Eric H. Kim, Lynette J. Tippett, Jean-Paul G. Vonsattel, and Richard LM Faull. "The Neuropathology of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 33–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_354.

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Carreira, João Casaca, Ali Jahanshahi, Dagmar Zeef, Ersoy Kocabicak, Rinske Vlamings, Stephan von Hörsten, and Yasin Temel. "Transgenic Rat Models of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 135–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_245.

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Li, Xiao-Jiang, and Shihua Li. "Large Animal Models of Huntington’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 149–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_246.

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Fellner, Lisa, Gregor K. Wenning, and Nadia Stefanova. "Models of Multiple System Atrophy." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 369–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7854_2013_269.

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Van der Perren, Anke, Chris Van den Haute, and Veerle Baekelandt. "Viral Vector-Based Models of Parkinson’s Disease." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 271–301. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_310.

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

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Dinesh, Karthik, Mulin Xiong, Jamie Adams, Ray Dorsey, and Gaurav Sharma. "Signal analysis for detecting motor symptoms in Parkinson's and Huntington's disease using multiple body-affixed sensors: A pilot study." In 2016 IEEE Western New York Image and Signal Processing Workshop (WNYISPW). IEEE, 2016. http://dx.doi.org/10.1109/wnyipw.2016.7904834.

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Aldaz, Tatiana, Pasquale Nigro, Celia Painous, Almudena Sánchez, and Esteban Muñoz. "F05 Prevalence of non-motor symptoms in huntington’s disease. a comparative study with parkinson’s disease." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.111.

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Kuosmanen, Elina, Valerii Kan, Julio Vega, Aku Visuri, Yuuki Nishiyama, Anind K. Dey, Simon Harper, and Denzil Ferreira. "Challenges of Parkinson's Disease." In MobileHCI '19: 21st International Conference on Human-Computer Interaction with Mobile Devices and Services. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3338286.3340133.

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Plerou, Antonia, Catherine Bobori, and Panayiotis Vlamos. "Molecular basis of Huntington's disease and brain imaging evidence." In 2015 IEEE International Symposium on Signal Processing and Information Technology (ISSPIT). IEEE, 2015. http://dx.doi.org/10.1109/isspit.2015.7394365.

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Mina, Eleni, Mark Thompson, Kristina M. Hettne, Willeke Van Roon-Mom, Rajaram Kaliyaperumal, Eelke Van Der Horst, Katherine Wolstencroft, Barend Mons, and Marco Roos. "Multidisciplinary Collaboration to Facilitate Hypotheses Generation in Huntington's Disease." In 2015 IEEE 11th International Conference on e-Science (e-Science). IEEE, 2015. http://dx.doi.org/10.1109/escience.2015.71.

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Neela, D., and K. Rangarajan. "Hybrid Workflow Net Based Architecture for Modeling Huntington's Disease." In 2011 Sixth International Conference on Bio-Inspired Computing: Theories and Applications (BIC-TA). IEEE, 2011. http://dx.doi.org/10.1109/bic-ta.2011.46.

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Torres, R., M. Huerta, R. Gonzalez, R. Clotet, J. Bermeo, and G. Vayas. "Sensors for Parkinson's disease evaluation." In 2017 International Caribbean Conference on Devices, Circuits and Systems (ICCDCS). IEEE, 2017. http://dx.doi.org/10.1109/iccdcs.2017.7959715.

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Graca, Ricardo, Rui Sarmento e Castro, and Joao Cevada. "ParkDetect: Early diagnosing Parkinson's Disease." In 2014 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2014. http://dx.doi.org/10.1109/memea.2014.6860027.

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Elcin, Huseyn. "PARKINSON'S DISEASE MEDICAL REHABILITATION METHODS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30062021/7623.

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Paula Felix, Juliana, Flavio Henrique Teles Vieira, Gabriel da Silva Vieira, Ricardo Augusto Pereira Franco, Ronaldo Martins da Costa, and Rogerio Lopes Salvini. "An Automatic Method for Identifying Huntington's Disease using Gait Dynamics." In 2019 IEEE 31st International Conference on Tools with Artificial Intelligence (ICTAI). IEEE, 2019. http://dx.doi.org/10.1109/ictai.2019.00243.

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Reports on the topic "Parkinson's disease; Huntington's disease"

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Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada493391.

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Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434051.

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3

Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada609645.

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Seroogy, Kim B., and David M. Yurek. Neuregulins, Neuroprotection and Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada415998.

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Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada416957.

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Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada609150.

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Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada511588.

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Nelson, Lorene M. Military Service and Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada583477.

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Tanner, Caroline M. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada562185.

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Tanner, Caroline M. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada609026.

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You might also be interested in the extended bibliographies on the topic 'Parkinson's disease; Huntington's disease' for particular source types:
Journal articles Dissertations / Theses Books
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