Relevant bibliographies by topics / Parkinson's disease, biomarkers, treatment

Academic literature on the topic 'Parkinson's disease, biomarkers, treatment'

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Published: 11 March 2023

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Journal articles on the topic "Parkinson's disease, biomarkers, treatment"

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Pilipovich, A. A., V. L. Golubev, Al B. Danilov, and R. R. Tyutina. "Role of biometals in pathogenesis treatment of Parkinson's disease (overview)." Medical alphabet, no. 1 (June 11, 2020): 21–27. http://dx.doi.org/10.33667/2078-5631-2020-1-21-27.

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The role of exogenous factors in the occurrence of neurodegenerative diseases has been shown in many works: on the effects of radiation, neurotoxicants, pesticides and other organic and inorganic substances. One of the interesting and promising areas for studying the pathogenesis of neurodegeneration is the analysis of the composition and ratio of trace elements in various tissues and organs of a person. The influence of trace elements on the development of neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease, amyotrophic lateral sclerosis, is given special attention, since such patients show multiple disorders in the homeostasis of the main endogenous brain biometals (calcium, magnesium, zinc, iron, manganese, copper, etc.). On the one hand, in a cell or its components, where metals play a key role in biological processes, a metal deficiency can occur, on the other hand, metals can accumulate in pathological proteins, causing cell dysfunction and death. Protein aggregation is a common feature of all neurodegenerative diseases. Specific changes in the concentration of biometals in various environments of the body can be considered as early biomarkers of neurodegenerations. And the identification of reliable biomarkers is considered a paramount task for the development of the direction of early therapy and prevention of the disease, in particular PD. A change in the distribution of metal, cell deficiency and sequestration in pathological proteins are abnormalities that must be addressed during neurodegeneration. Currently, approximately 800 compounds are used or tested for the treatment of PD, of which approximately 250 have the expected or established chelation properties of metals (CuII, CuI, FeII, FeIII, MnII, ZnII) that are involved in dyshomeostasis in PD. Today's knowledge of the pathogenesis of the most common neurodegenerations, such as AD and PD, is still not enough to develop clear recommendations for therapy with biometals and other trace elements, but work in this direction is actively ongoing.
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Svenningsson, Per, Eric Westman, Clive Ballard, and Dag Aarsland. "Cognitive impairment in patients with Parkinson's disease: diagnosis, biomarkers, and treatment." Lancet Neurology 11, no. 8 (August 2012): 697–707. http://dx.doi.org/10.1016/s1474-4422(12)70152-7.

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Raghunathan, Rekha, Kathleen Turajane, and Li Chin Wong. "Biomarkers in Neurodegenerative Diseases: Proteomics Spotlight on ALS and Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 16 (August 18, 2022): 9299. http://dx.doi.org/10.3390/ijms23169299.

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Neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD) are both characterized by pathogenic protein aggregates that correlate with the progressive degeneration of neurons and the loss of behavioral functions. Both diseases lack biomarkers for diagnosis and treatment efficacy. Proteomics is an unbiased quantitative tool capable of the high throughput quantitation of thousands of proteins from minimal sample volumes. We review recent proteomic studies in human tissues, plasma, cerebrospinal fluid (CSF), and exosomes in ALS and PD that identify proteins with potential utility as biomarkers. Further, we review disease-related post-translational modifications in key proteins TDP43 in ALS and α-synuclein in PD studies, which may serve as biomarkers. We compare relative and absolute quantitative proteomic approaches in key biomarker studies in ALS and PD and discuss recent technological advancements which may identify suitable biomarkers for the early-diagnosis treatment efficacy of these diseases.
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Frutos, Laura López de, Francisco Almeida, Jessica Murillo-Saich, Vasco A. Conceição, Monica Guma, Oswald Queheberger, Pilar Giraldo, and Gabriel Miltenberger-Miltenyi. "Serum Phospholipid Profile Changes in Gaucher Disease and Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 18 (September 8, 2022): 10387. http://dx.doi.org/10.3390/ijms231810387.

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Alterations in the levels of serum sphingolipids and phospholipids have been reported in Gaucher disease and in Parkinson’s disease, suggesting a potential role of these lipids as biomarkers. This project’s objective is to detect novel associations and novel candidate biomarkers in the largest Spanish Gaucher and Parkinson diseases of the Iberian Peninsula. For that, 278 participants were included: 100 sporadic Parkinson’s patients, 70 Gaucher patients, 15 GBA1-mutation-carrier Parkinson’s patients and 93 controls. A serum lipidomics array including 10 phospholipid groups, 368 species, was performed using high-performance liquid chromatography–mass spectrometry. Lipid levels were compared between groups via multiple-regression analyses controlling for clinical and demographic parameters. Additionally, lipid levels were compared within the Gaucher and Parkinson’s groups controlling for medication and/or disease severity. Results were controlled for robustness by filtering of non-detectable lipid values. There was an increase in the levels of phosphatidylcholine, with a simultaneous decrease in lyso-phosphatidylcholine, in the Gaucher, Parkinson’s and GBA1-mutation-carrier Parkinson’s patients vs. controls. Phosphatidylethanolamine, lyso- and plasmalogen-phosphatidylethanolamine were also increased in Gaucher and Parkinson’s. Gaucher patients also showed an increase in lyso-phosphatidylserine and phosphatidylglycerol. While in the Gaucher and Parkinson’s groups, velaglucerase alpha and dopamine agonists, respectively, showed positive associations with the lipid changes, miglustat treatment in Gaucher patients normalized the altered phosphatidylcholine/lyso-phosphatidylcholine ratio. In conclusion, Gaucher and Parkinson’s patients showed changes in various serum phospholipid levels when compared with healthy controls, further supporting the role of such lipids in disease development and, possibly, as putative biomarkers. This hypothesis was reinforced by the normalizing effect of miglustat, and by controlling for data robustness, even though the limited number of participants, especially in the sub-distribution by treatment groups in GD requires validation in a larger number of patients.
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Polissidis, Alexia, Lilian Petropoulou-Vathi, Modestos Nakos-Bimpos, and Hardy J. Rideout. "The Future of Targeted Gene-Based Treatment Strategies and Biomarkers in Parkinson’s Disease." Biomolecules 10, no. 6 (June 16, 2020): 912. http://dx.doi.org/10.3390/biom10060912.

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Biomarkers and disease-modifying therapies are both urgent unmet medical needs in the treatment of Parkinson’s disease (PD) and must be developed concurrently because of their interdependent relationship: biomarkers for the early detection of disease (i.e., prior to overt neurodegeneration) are necessary in order for patients to receive maximal therapeutic benefit and vice versa; disease-modifying therapies must become available for patients whose potential for disease diagnosis and prognosis can be predicted with biomarkers. This review provides an overview of the milestones achieved to date in the therapeutic strategy development of disease-modifying therapies and biomarkers for PD, with a focus on the most common and advanced genetically linked targets alpha-synuclein (SNCA), leucine-rich repeat kinase-2 (LRRK2) and glucocerebrosidase (GBA1). Furthermore, we discuss the convergence of the different pathways and the importance of patient stratification and how these advances may apply more broadly to idiopathic PD. The heterogeneity of PD poses a challenge for therapeutic and biomarker development, however, the one gene- one target approach has brought us closer than ever before to an unprecedented number of clinical trials and biomarker advancements.
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Russillo, Maria Claudia, Valentina Andreozzi, Roberto Erro, Marina Picillo, Marianna Amboni, Sofia Cuoco, Paolo Barone, and Maria Teresa Pellecchia. "Sex Differences in Parkinson’s Disease: From Bench to Bedside." Brain Sciences 12, no. 7 (July 13, 2022): 917. http://dx.doi.org/10.3390/brainsci12070917.

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Background: Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease and gender differences have been described on several aspects of PD. In the present commentary, we aimed to collect and discuss the currently available evidence on gender differences in PD regarding biomarkers, genetic factors, motor and non-motor symptoms, therapeutic management (including pharmacological and surgical treatment) as well as preclinical studies. Methods: A systematic literature review was performed by searching the Pubmed and Scopus databases with the search strings “biomarkers”, “deep brain stimulation”, “female”, “gender”, “genetic”, “levodopa”, “men”, “male”, “motor symptoms”, “non-motor symptoms”, “Parkinson disease”, “sex”, “surgery”, and “women”. Results: The present review confirms the existence of differences between men and women in Parkinson Disease, pointing out new information regarding evidence from animal models, genetic factors, biomarkers, clinical features and pharmacological and surgical treatment. Conclusions: The overall goal is to acquire new informations about sex and gender differences in Parkinson Disease, in order to develop tailored intervetions.
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Redenšek, Sara, and Vita Dolžan. "The role of pharmacogenomics in the personalization of Parkinson's disease treatment." Pharmacogenomics 21, no. 14 (September 2020): 1033–43. http://dx.doi.org/10.2217/pgs-2020-0031.

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Parkinson's disease (PD)-related phenotypes can vary among patients substantially, including response to dopaminergic treatment in terms of efficacy and occurrence of adverse events. Many pharmacogenetic studies have already been conducted to find genetic markers of response to dopaminergic treatment. Integration of genetic and clinical data has already resulted in construction of clinical pharmacogenetic models for prediction of adverse events. However, the results of pharmacogenetic studies are inconsistent. More comprehensive genome-wide approaches are needed to find genetic biomarkers of PD-related phenotypes to better explain the variability in response to treatment. These genetic markers should be integrated with clinical, environmental, imaging, and other omics data to build clinically useful algorithms for personalization of PD management.
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Kwon, Eun Hae, Sabrina Tennagels, Ralf Gold, Klaus Gerwert, Léon Beyer, and Lars Tönges. "Update on CSF Biomarkers in Parkinson’s Disease." Biomolecules 12, no. 2 (February 18, 2022): 329. http://dx.doi.org/10.3390/biom12020329.

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Progress in developing disease-modifying therapies in Parkinson’s disease (PD) can only be achieved through reliable objective markers that help to identify subjects at risk. This includes an early and accurate diagnosis as well as continuous monitoring of disease progression and therapy response. Although PD diagnosis still relies mainly on clinical features, encouragingly, advances in biomarker discovery have been made. The cerebrospinal fluid (CSF) is a biofluid of particular interest to study biomarkers since it is closest to the brain structures and therefore could serve as an ideal source to reflect ongoing pathologic processes. According to the key pathophysiological mechanisms, the CSF status of α-synuclein species, markers of amyloid and tau pathology, neurofilament light chain, lysosomal enzymes and markers of neuroinflammation provide promising preliminary results as candidate biomarkers. Untargeted approaches in the field of metabolomics provide insights into novel and interconnected biological pathways. Markers based on genetic forms of PD can contribute to identifying subgroups suitable for gene-targeted treatment strategies that might also be transferable to sporadic PD. Further validation analyses in large PD cohort studies will identify the CSF biomarker or biomarker combinations with the best value for clinical and research purposes.
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Camicioli, Richard, and Serge Gauthier. "Clinical Trials in Parkinson's Disease Dementia and Dementia with Lewy Bodies." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 34, S1 (March 2007): S109—S117. http://dx.doi.org/10.1017/s0317167100005679.

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Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB) are pathological overlapping and important causes of dementia for which clinical trials are in their infancy. Cholinesterase inhibitors may be of benefit in DLB and PDD, as suggested by placebo-controlled clinical trials of rivastigmine and donepezil. The anti-psychotic agent clozapine has been of benefit in PD and PDD, but other agents, such as quetiapine, require adequate assessment. Barriers to trials include pathological overlap that can lead to inaccuracies in clinical diagnosis, unavailability of a consensus definition for PDD, unanswered questions regarding natural history and the paucity of validated outcome measures. Motor impairment must be considered in patients with PDD and DLB; conversely, cognitive impairment should be assessed in trials targeting motor impairment in advanced PD. Potential targets for treatment include onset of dementia, cognitive impairment, behavioral impairment, functional decline, falls, nursing home placement, mortality, quality of life and economic impact. Biomarkers including neuroimaging and cerebrospinal fluid markers are not currently established. At present PDD and DLB are distinct entities by definition. Future studies, including clinical trials and biomarker studies, will help to further define the clinical and therapeutic implications of this distinction.
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Lee, Ju-Young, Hyeo-il Ma, and Young Eun Kim. "Biomarker in Parkinson’s Disease: Clinical and Biochemical Biomarker." Journal of the Korean Neurological Association 39, no. 4 (November 1, 2021): 287–97. http://dx.doi.org/10.17340/jkna.2021.4.4.

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Parkinson’s disease is a neurodegenerative disease compromising progressive motor and non-motor features for a long disease course. Although many drugs controlling parkinsonian symptoms were discovered, treatment with disease-modifying or halting effect was not developed to date. The exploration of reliable biomarkers would be helpful for better predicting disease progression and thereby successful development of disease-modifying therapy. In this review, we will review the clinical biomarkers in the prodromal stage and biomarkers using biological tissue in Parkinson’s disease.
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Dissertations / Theses on the topic "Parkinson's disease, biomarkers, treatment"

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Luan, Hemi. "Mass spectrometry based metabolomics for biomarkers of Parkinson's disease." HKBU Institutional Repository, 2017. https://repository.hkbu.edu.hk/etd_oa/396.

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Increasing evidence has shown that abnormal metabolic phenotypes in body fluids reflect the pathogenesis and pathophysiology of Parkinson's disease (PD). However, the relationship between metabolic phenotypes and PD is not fully understood. Mass spectrometry (MS) based metabolomics is a powerful technique, which was frequently used for the sensitive and reproducible detection of hundreds to thousands of metabolites in biofluid samples.. Here we developed and performed MS-based metabolomics studies involving hundreds of human urine samples with data acquired from multiple analytical batches for surveying potential biomarkers of PD. A new software statTarget was developed and introduced. Protocols for liquid chromatography-mass spectrometry (LC-MS) and gas chromatography-mass spectrometry (GC-MS) were developed, including sample preparation, data acquisition, quality controls, quality assurance and data analysis. Urinary metabolites from a total of 401 clinical urine samples collected from 106 idiopathic PD patients and 104 normal control subjects were profiled by using LC-MS. Quality control (QC) strategy has been performed in MS-based metabolomics for high reproducibility and accuracy of MS data. GC-MS with methyl chloroformate (MCF) derivatization was used for profiling highly polar metabolites in patients with early-, middle- and advanced-stage PD. Our study revealed the significant correlation between clinical phenotypes and urinary metabolite profiles. Comprehensive metabolomics was successfully developed with the goal of identifying urinary metabolite markers that can be used for evaluating the development of PD. A group of 18 metabolites have shown not only a high discriminating ability for the early-stage PD patients but also accurately distinguished the middle- and advanced- stages patients from control subjects. For the evaluation of PD, 18 metabolites showed good potential as metabolite markers with related metabolic pathway variations observed in branched chain amino acid metabolism, glycine derivation, steroid hormone biosynthesis, tryptophan metabolism, and phenylalanine metabolism.. We have further performed targeted analysis of potential biomarkers by using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and GC-MS. The UPLC-MS/MS method was developed and optimized for detecting the concentration variation of metabolites in tryptophan metabolism for alpha-synuclein over-expressed flies (Parkinson's disease model). The altered tryptophan metabolism was proved as one of the common metabolite signatures between PD patients and alpha-synuclein over-expressed fly model of PD, and thus may be used for developing potential markers of the disease and evaluating the efficacy of novel therapeutic agents. An asymmetric labeling strategy and positive chemical ionization gas chromatography-tandem mass spectrometry (PCI-GC-MS-MS) approach was developed for the determination of non-amino organic acids and amino acids, as well as short chain fatty acids. Carboxylic and amino groups could be selectively labelled by propyl and ethyl groups, respectively. The specific neutral losses of C3H8O (60 Da), C3H5O2 (74 Da) and C4H8O2 (88 Da) were useful in the selective identification for qualitative analysis of organic acids and amino acid derivatives. The developed PCI-GC-MS/MS method showed good reproducibility and linear range.. In summary, metabolomics study has its inherent advantage in the characterization of biomarkers for the development of PD and may bring new scientific knowledge as well as impact on the progression of PD and other related neurodegenerative diseases.
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Han, Brent. "Biomarkers of progression in mirroring models of Parkinson's disease." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453005.

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Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed June 25, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 34-37).
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Tabatabaei, Ali Reza. "Parkinson's disease : etiology, prevention and treatment." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30382.

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This thesis consists of three chapters dealing with different aspects of Parkinson's disease (PD). 3-Acetylpyridine (3-AP), a naturally occurring neurotoxin, was studied for its neurodegenerative properties on the mesostriatal dopaminergic system in rats as a possible environmental cause of idiopathic PD. Chronic administration of this compound to rats caused a moderate but insignificant reduction of striatal dopamine (determined by HPLC measurement of striatal dopamine) and a more substantial degeneration of cerebellar neurons and their neurotransmitters (determined by amino acid analysis of cerebellum). Prophylactic use of a high dose of nicotinamide prevented the reduction of dopamine in the striatum as well as the severe behavioural manifestations induced by 3-AP in rats. The cerebellar damage, however, was not affected. Different mechanisms of damage by 3-AP in these structures were presumed based on the protective effects of nicotinamide in the substantia nigra but not in the cerebellum. Possible protective properties of MK-801 (a noncompetitive NMDA antagonist) and nicotinamide against MPTP neurotoxicity were also examined in mice. MK-801 treatment provided a substantial protection against MPTP-induced reduction of striatal dopamine. Nicotinamide on the other hand provided no such protection. Finally, a new controversial approach to the treatment of parkinsonism was evaluated. Nervous tissue from 13-15 day-old fetuses was transplanted into MPTP-treated mice. The transplanted material was harvested from different areas of the fetal brain and was prepared by various procedures to examine the possible bases of any improvement in the host animal. After two studies, we did not find a biochemical improvement in transplanted mice treated with MPTP regardless of the nature of the transplanted materials.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Athauda, Dilan Sampath. "Exenatide and the treatment of Parkinson's disease." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10053514/.

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of people over the age of 65. Despite the best available medical and surgical therapies, there are no known treatments that can slow or alter clinical disease progression or continued neurodegeneration, thus any novel intervention that could delay or slow progression of PD would provide much needed health and socio-economic benefits. The mechanisms underlying PD pathogenesis remain unclear but there is accumulating evidence to suggesting that Type 2 diabetes and PD, both age-related diseases, share similar dysfunctional pathways. Alterations in metabolism, inflammation and mitochondrial function occur in both diseases and growing evidence suggests these pathways may impact on various tissues’ ability to respond to insulin, leading to “insulin resistance” in peripheral tissues and neurones, promoting cell death pathways and leading ultimately to diabetes and neurodegeneration respectively. The common pathways between these two conditions has led some to speculate that “insulin sensitizing” treatments for patients with Type 2 diabetes may be useful as novel treatments in neurodegenerative diseases such as PD. Exenatide is a Glucagon-like peptide-1 (GLP-1) agonist, currently licensed for the treatment for Type 2 diabetes and acts on insulin signalling pathways. It has demonstrated neuroprotective effects across a variety of animal toxin models of PD and also in a proof of concept, open label trial of mid-stage PD patients, conferring persistent motor and cognitive benefits sustained past the period of drug exposure. In this thesis I will present the first data from a fully randomised, placebo-controlled trial of exenatide in PD patients and explore the effects of exenatide on disease progression in PD and its influence on motor and non-motor symptoms. Furthermore, I will explore the pharmacokinetics of exenatide in this population and, utilising data from serum extracellular vesicles (exosomes) enriched for neuronal origin from the Exenatide-PD trial participants, demonstrate that peripherally administered exenatide can engage with neuronal insulin signalling pathways, providing some mechanistic context for the trial results. Taken together, data presented here will provide compelling evidence supporting the links between insulin signalling and PD and that the role of exenatide and other GLP-1 agonists as a novel treatment for PD should be explored further.
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Aviles-Olmos, I. "Exenatide as a novel treatment for Parkinson's Disease." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415695/.

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PD is a progressive neurodegenerative disease that results in intolerable disability for most patients despite the best current medical and surgical therapies. A treatment that slows, or stops clinical progression is the major therapeutic goal of current PD research. Multiple avenues of research including epidemiology, molecular genetics and cell biology have identified links between Parkinson’s disease (PD) and Type 2 diabetes mellitus (T2DM). Several recent discoveries have highlighted common cellular pathways that potentially relate neurodegenerative processes with abnormal mitochondrial function and abnormal glucose metabolism. In parallel with these advances, a treatment for insulin resistance (Exenatide) has been evaluated as a possible disease modifying drug in PD, which forms the core of my PhD. Exenatide is the synthetic version of Exendin-4, confirmed to be an agonist of the Glucagon-like-peptide-1 (GLP-1) receptor, and resistant to the normal GLP-1 enzymatic degradation processes. The aim of this thesis is the evaluation of Exenatide’s possible role as a potential neuroprotective/disease modifying agent in PD (with only preliminary insights regarding its mechanisms of action in neurodegeneration). This study presents the following data: 1. Methods used to obtained proof of concept data from patients with moderate PD treated with Exenatide to provide preliminary support for its further study. 2. An exploration of possible objective measures of differences resulting from Exenatide exposure in a PD biomarker- SPECT imaging, using statistical parametric mapping of a subgroup of patients treated with Exenatide. 3. Prolonged follow up of these patients to further try and help distinguish placebo effects from possible biological effects of Exenatide in PD. 4. An attempt to identify a possible mechanism of action of Exenatide in our cohort of patients. Glucose tolerance tests were performed as an indirect measure of insulin resistance.
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Wang, Michelle J. "Predictive ability of cerebrospinal fluid biomarkers in diagnosing and evaluating Parkinson's disease." Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/92059.

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Thesis: M. Eng., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2014.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (page 31).
Currently, there are a variety of clinical assessments and rating scales used in the research and treatment of Parkinson's disease (PD). Despite the widespread use and reliance on these scales, they do not offer a uniform, objective measure. Many previous studies have indicated promising relationships between various biomarkers and Parkinsonian symptoms that could lead to objective measures by using statistical methods and providing p-values. However, we could not find any literature that uses machine learning or directly tests predictive value. The goal of this thesis was to determine whether or not cerebrospinal fluid (CSF) biomarker data could predict incidence of Parkinson's with a high degree of accuracy and differentiate between patients with varying levels of severity. We used various supervised machine learning algorithms on the Parkinson's Progression Markers Initiative (PPMI) baseline data set provided by the Michael J. Fox Foundation, and reported the percentage of patients correctly diagnosed by each algorithm on an isolated test data set. The best classifier averaged 69% accuracy in distinguishing human controls from PD patients. While this does indicate the presence of some predictive power, it is not clinically useful and we tentatively conclude a negative result. The data pertain to the CSF biomarkers available from PPMI at the end of October 2013.
by Michelle J. Wang.
M. Eng.
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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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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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Rittman, Timothy. "Connectivity biomarkers in neurodegenerative tauopathies." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/248866.

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The primary tauopathies are a group of neurodegenerative diseases affecting movement and cognition. In this thesis I study Progressive Supranuclear Palsy (PSP) and the Corticobasal Syndrome (CBS), two parkinsonian disorders associated with accumulation of hyperphos- phorylated and abnormally folded tau protein. I contrast these two disorders with Parkinson’s disease (PD), which is associated with the accumulation of alpha-synuclein but has a genetic association with the MAPT gene encoding tau. Understanding the tauopathies to develop effective treatments will require a better grasp of the relationships between clinical syndromes and cognitive measures and how the anatomical and neurochemical networks that underlie clinical features might be altered by disease. I investigate simple clinical biomarkers, showing that a two-minute test of verbal fluency is a potential diagnostic biomarker to distinguish between PD and PSP and that the ACE-R and its subscores could play a role in monitoring cognition over time in PD, PSP and CBS. I assess the implementation of network analysis in Functional Mag- netic Resonance Imaging (fMRI) data, introduce Maybrain software for graphical network analysis and visualisation. I go on to show an overlap between graph theory network measures and I identify three main factors underlying graph network measures of: efficiency and distance, hub characteristics, network community measures. I apply these measures in PD, PSP and the CBS. All three diseases caused a loss of functional connectivity in com- parison to the control group that was concentrated in more highly connected brain regions and in longer distance connections. In ad- dition, widely localised cognitive function of verbal fluency co-varied with the connection strength in highly connected regions across PD, PSP and CBS. To take this further, I investigated specific functional covariance networks. All three disease groups showed reduced connectivity between the basal ganglia network and other networks, and between the anterior salience network and other networks. Localised areas of increased co- variance suggest a breakdown of network boundaries which correlated with motor severity in PSP and CBS, and duration of disease in CBS. I explore the link between gene expression of the tau gene MAPT and its effects on functional connectivity showing that the expression of MAPT correlated with connection strength in highly connected hub regions that were more susceptible to a loss of connection strength in PD and PSP. I conclude by discussing how tau protein aggregates and soluble tau oligomers may explain the changes in functional brain networks. The primary tauopathies are a group of neurodegenerative diseases affecting movement and cognition. In this thesis I study Progressive Supranuclear Palsy (PSP) and the Corticobasal Syndrome (CBS), two parkinsonian disorders associated with accumulation of hyperphos- phorylated and abnormally folded tau protein. I contrast these two disorders with Parkinson’s disease (PD), which is associated with the accumulation of alpha-synuclein but has a genetic association with the MAPT gene encoding tau. Understanding the tauopathies to develop effective treatments will require a better grasp of the relationships between clinical syndromes and cognitive measures and how the anatomical and neurochemical networks that underlie clinical features might be altered by disease. I investigate simple clinical biomarkers, showing that a two-minute test of verbal fluency is a potential diagnostic biomarker to distinguish between PD and PSP and that the ACE-R and its subscores could play a role in monitoring cognition over time in PD, PSP and CBS. I assess the implementation of network analysis in Functional Mag- netic Resonance Imaging (fMRI) data, introduce Maybrain software for graphical network analysis and visualisation. I go on to show an overlap between graph theory network measures and I identify three main factors underlying graph network measures of: efficiency and distance, hub characteristics, network community measures. I apply these measures in PD, PSP and the CBS. All three diseases caused a loss of functional connectivity in com- parison to the control group that was concentrated in more highly connected brain regions and in longer distance connections. In ad- dition, widely localised cognitive function of verbal fluency co-varied with the connection strength in highly connected regions across PD, PSP and CBS. To take this further, I investigated specific functional covariance networks. All three disease groups showed reduced connectivity between the basal ganglia network and other networks, and between the anterior salience network and other networks. Localised areas of increased co- variance suggest a breakdown of network boundaries which correlated with motor severity in PSP and CBS, and duration of disease in CBS. I explore the link between gene expression of the tau gene MAPT and its effects on functional connectivity showing that the expression of MAPT correlated with connection strength in highly connected hub regions that were more susceptible to a loss of connection strength in PD and PSP. I conclude by discussing how tau protein aggregates and soluble tau oligomers may explain the changes in functional brain networks.
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Yarnall, Alison Jane. "Predicting cognitive impairment in Parkinson's disease using neurophysiology and biochemical parameters as biomarkers." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2278.

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Parkinson’s disease (PD) is a common neurodegenerative condition with multiple associated non-motor symptoms. Of these, dementia is a frequent debilitating complication of the disorder, with significant morbidity and mortality. Some forms of mild cognitive impairment in PD (PD-MCI) may represent a pre-dementia state and certain clinical, laboratory and neurophysiological parameters may increase the accuracy of prediction of cognitive decline. If validated, these markers would offer the opportunity for disease modification and therapeutic intervention at a critical early stage of the illness, when the viable neuronal population is greater. The key aim of this thesis was to characterise cognitive impairment in PD in a cohort of newly diagnosed cases, and evaluate how a panel of biomarkers correlated with cognitive phenotypes to predict risk of future cognitive decline. The main findings were that PD-MCI was common, and was associated with a distinct clinical phenotype. Memory impairment was the most common single domain affected, although the majority of those with PD-MCI were classified as nonamnestic single domain subtype. A significant correlation was found between pattern recognition memory, sensitive to temporal lobe impairments, and cerebrospinal amyloid-β 1-42 levels, thought to represent amyloid-β metabolism and deposition Both amyloid-β 1-42 and 1-40 levels were significantly lower in those with impaired cognition. In addition, short latency afferent inhibition, a neurophysiological in vivo non-invasive measurement of cholinergic function, was also reduced in participants with mild cognitive impairment. These findings suggest that cholinergic dysfunction and amyloid deposition may contribute to the underlying pathophysiology of early PD- MCI. The major conclusion from this thesis is that PD-MCI is heterogeneous and more frequent than previously reported in early disease. This is associated with abnormalities of amyloid processing and cholinergic dysfunction, and may highlight those at risk of developing dementia. Longitudinal assessment of these individuals will enable us to determine and better model those measures predictive of cognitive decline at an early disease stage.
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Books on the topic "Parkinson's disease, biomarkers, treatment"

1

Grimes, J. David. Parkinson's disease. Dorval, Quebec: Sandoz Canada, 1985.

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E, Lyons Kelly, ed. Treatment decisions in Parkinson's disease. New York: Oxford University Press, 2010.

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Peter, LeWitt, and Oertel Wolfgang H, eds. Parkinson's disease: The treatment options. London: Martin Dunitz, 1999.

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McCall, Bridget. Living with Parkinson's disease. London: Sheldon, 2006.

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1945-, Koller William C., and Paulson George W. 1930-, eds. Therapy of Parkinson's disease. New York: M. Dekker, 1990.

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Rajesh, Pahwa, Lyons Kelly E, and Koller William C. 1945-, eds. Therapy of Parkinson's disease. 3rd ed. New York: M. Dekker, 2004.

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I, Caird F., ed. Rehabilitation in Parkinson's disease. London: Chapman and Hall, 1991.

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1941-, Olanow C. W., ed. Principles of treatment in Parkinson's disease. Philadelphia, PA: Butterworth-Heinemann/Elsevier, 2005.

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Parkinson's disease treatment guide for physicians. New York: Oxford University Press, 2009.

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Yoshida, Chiyo, and Ami Ito. Parkinson's disease: Diagnosis, treatment, and prognosis. New York: Nova Science Publishers, Inc., 2012.

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Book chapters on the topic "Parkinson's disease, biomarkers, treatment"

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Krokidis, Marios G., Themis Exarchos, and Panayiotis Vlamos. "Bioinformatics Approaches for Parkinson’s Disease in Clinical Practice: Data-Driven Biomarkers and Pharmacological Treatment." In GeNeDis 2020, 193–98. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78775-2_23.

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Emre, Murat. "Treatment of Dementia Associated with Parkinson's Disease." In Parkinson's Disease, 163–69. Oxford, UK: Blackwell Publishing Ltd., 2011. http://dx.doi.org/10.1002/9781444397970.ch15.

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Fox, Susan H., and Jonathan M. Brotchie. "Non-Dopaminergic Approaches to the Treatment of Parkinson's Disease." In Parkinson's Disease, 432–54. Oxford, UK: Blackwell Publishing Ltd., 2011. http://dx.doi.org/10.1002/9781444397970.ch38.

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Stacy, Mark, and Joseph Jankovic. "Overview of the Medical Treatment of the Non-Motor and Non-Dopaminergic Features of Parkinson's Disease." In Parkinson's Disease, 394–408. Oxford, UK: Blackwell Publishing Ltd., 2011. http://dx.doi.org/10.1002/9781444397970.ch35.

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Dalvi, Arif, Kelly E. Lyons, and Rajesh Pahwa. "Parkinson’s Disease: An Overview of Etiology, Clinical Manifestations, and Treatment." In Inflammation in Parkinson's Disease, 1–24. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08046-8_1.

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Child, Nicholas D., and Bryan T. Klassen. "Evidence-based treatment of Parkinson's disease." In Evidence-Based Neurology: Management of Neurological Disorders, 191–208. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119067344.ch19.

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Rascol, Olivier, and Regina Katzenschlager. "The Treatment of Early Parkinson's Disease." In Therapeutics of Parkinson's Disease and Other Movement Disorders, 49–70. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470713990.ch4.

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Ruiz-Lancheros, Elizabeth, Eric Chatelain, and Momar Ndao. "Chagas Disease Treatment Efficacy Biomarkers: Myths and Realities." In Chagas Disease, 323–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-00054-7_16.

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Katzenschlager, Regina. "Pharmacological Treatment Options for Levodopa-Induced Dyskinesia." In Levodopa-Induced Dyskinesia in Parkinson's Disease, 69–88. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6503-3_5.

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Parnetti, Lucilla, Anna Castrioto, Claudia De, Davide Chiasserini, Nicola Tambasco, Aroldo Rossi, Chiara Balducci, Tommaso Beccari, and Paolo Calabresi. "CFS Biomarkers in Parkinson’s Disease." In Diagnosis and Treatment of Parkinson's Disease. InTech, 2011. http://dx.doi.org/10.5772/16666.

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Conference papers on the topic "Parkinson's disease, biomarkers, treatment"

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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa, and Edvaldo Cardoso. "Brain-gut-microbiota axis in motor disorders." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.401.

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Introduction: There seems to be a strong relationship and influence on the brain-gut- microbiota axis in the control and prevention of several diseases, including degenerative diseases that are related to motor disorders. Objectives: To analyze the relationship between movement disorders and the intestinal microbiota. Methods: Integrative review performed at PUBMED, using the descriptors Movement disorder and intestinal microbiota, in the last five years and having as inclusion criteria complete texts in English. Results: The literature suggests that the intestinal microbiota regulates the activation of microglia through the production of bacteria metabolites. Gut dysbiosis is believed to generate metabolic disorders with decreased production of neuroprotective factors, increased pro-inflammatory cytokines, production of neurotoxins, and a misdirected immune response. Metabolites produced by an altered microbiota seem to enter the circulation and affect neurological function. Braak’s hypothesis postulates that aberrant accumulation of α-synuclein (αSyn), a central component of the pathophysiology of Parkinson’s disease (PD), begins in the intestine and propagates through the vagus nerve to the brain, given that αSyn inclusions previously arise in the enteric nervous system and glossopharyngeal and vagus nerves, and vagotomized individuals have reduced risk of PD. Conclusion: The identification of the microbiota or its altered metabolites may serve as biomarkers, or even drug targets for the treatment of diseases of the central nervous system. The microbiota can be modulated through antibiotic therapy, fecal microbiota transplantation, prebiotic supplementation, dietary interventions and many other potential methods.
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Prashanth, R., S. Dutta Roy, S. Ghosh, and Pravat K. Mandal. "Shape features as biomarkers in early Parkinson's disease." In 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2013. http://dx.doi.org/10.1109/ner.2013.6695985.

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Hourani, Mou'ath, Alexandre Mendes, Regina Berretta, Pablo Moscato, Tuan D. Pham, and Xiaobo Zhou. "Genetic biomarkers for brain hemisphere differentiation in Parkinson's Disease." In COMPUTATIONAL MODELS FOR LIFE SCIENCES/CMLS '07. AIP, 2007. http://dx.doi.org/10.1063/1.2816624.

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Yu, Zeyang, Wael Asaad, Arto Nurmikko, Ilker Ozden, and Ilker Ozden. "Optogenetics-based neuromodulation for the treatment of Parkinson's disease." In 2017 International Conference on Intelligent Informatics and Biomedical Sciences (ICIIBMS). IEEE, 2017. http://dx.doi.org/10.1109/iciibms.2017.8279731.

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Vega, Julio, Caroline Jay, Markel Vigo, and Simon Harper. "Unobtrusive Monitoring of Parkinson's Disease Based on Digital Biomarkers of Human Behaviour." In ASSETS '17: The 19th International ACM SIGACCESS Conference on Computers and Accessibility. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3132525.3134782.

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Krause, Markus, Jan Smeddinck, and Ronald Meyer. "A digital game to support voice treatment for parkinson's disease." In CHI '13 Extended Abstracts on Human Factors in Computing Systems. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2468356.2468435.

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Naranjo, Claudia Carricarte, Connie Marras, Naomi P. Visanji, David J. Cornforth, Lazaro Sanchez-Rodriguez, Birgitt Schule, Samuel M. Goldman, et al. "Heart rate variability biomarkers of leucine-rich repeat kinase 2-associated Parkinson's disease." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158194.

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Kim, Mansu, Ji Hye Won, Jisu Hong, Junmo Kwon, Hyunjin Park, and Li Shen. "Deep Network-Based Feature Selection for Imaging Genetics: Application to Identifying Biomarkers for Parkinson's Disease." In 2020 IEEE 17th International Symposium on Biomedical Imaging (ISBI). IEEE, 2020. http://dx.doi.org/10.1109/isbi45749.2020.9098471.

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Zhang, Hairong, Carlos Sierra, Nancy Kwon, Marian Eleni Karakatsani, Vernice R. Jackson-Lewis, Serge Przedborski, and Elisa Konofagou. "Focused-ultrasound Mediated Anti-Alpha-Synuclein Antibody Delivery for the Treatment of Parkinson's Disease." In 2018 IEEE International Ultrasonics Symposium (IUS). IEEE, 2018. http://dx.doi.org/10.1109/ultsym.2018.8579677.

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Ruonala, V., E. Pekkonen, S. Rissanen, O. Airaksinen, G. Miroshnichenko, M. Kankaanpaa, and P. Karjalainen. "Dynamic tension EMG to characterize the effects of DBS treatment of advanced Parkinson's disease." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944315.

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Reports on the topic "Parkinson's disease, biomarkers, treatment"

1

Potashkin, Judith. Splice Variant Biomarkers for Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada600497.

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Hallett, Mark, Mikhail P. Lomarev, Sarah P. Richardson, Eric Wassermann, William Bara, and Grisel Lopez. Trials of Transcranial Stimulation for the Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada470897.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada397751.

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Gloricso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada407633.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, December 1999. http://dx.doi.org/10.21236/ada375299.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada383307.

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Hallett, Mark. Placebo Controlled Study of Repetitive Transcranial Magnetic Stimulation for the Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada434733.

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Hallett, Mark. Placebo Controlled Study of Repetitive Transcranial Magnetic Stimulation for the Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada421927.

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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

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Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
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Jun, Purumea, HuiYan Zhao, Ojin Kwon, and Jung-Hee Jang. Efficacy of traditional herbal medicine treatment based on pattern identification for idiopathic Parkinson's disease: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0020.

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