Relevant bibliographies by topics / MitoPark

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  2. Dissertations / Theses
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Academic literature on the topic 'MitoPark'

Author: Grafiati
Published: 10 September 2021
Last updated: 18 February 2022

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Journal articles on the topic "MitoPark"

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Hong, Chien-Tai, Kai-Yun Chen, Weu Wang, Jing-Yuan Chiu, Dean Wu, Tsu-Yi Chao, Chaur-Jong Hu, Kai-Yin Chau, and Oluwaseun Bamodu. "Insulin Resistance Promotes Parkinson’s Disease through Aberrant Expression of α-Synuclein, Mitochondrial Dysfunction, and Deregulation of the Polo-Like Kinase 2 Signaling." Cells 9, no. 3 (March 17, 2020): 740. http://dx.doi.org/10.3390/cells9030740.

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Background: Insulin resistance (IR), considered a hallmark of diabetes at the cellular level, is implicated in pre-diabetes, results in type 2 diabetes, and negatively affects mitochondrial function. Diabetes is increasingly associated with enhanced risk of developing Parkinson’s disease (PD); however, the underlying mechanism remains unclear. This study investigated the probable culpability of IR in the pathogenesis of PD. Methods: Using MitoPark mice in vivo models, diabetes was induced by a high-fat diet in the in vivo models, and IR was induced by protracted pulse-stimulation with 100 nM insulin treatment of neuronal cells, in vitro to determine the molecular mechanism(s) underlying altered cellular functions in PD, including mitochondrial dysfunction and α-synuclein (SNCA) aberrant expression. Findings: We observed increased SNCA expression in the dopaminergic (DA) neurons of both the wild-type and diabetic MitoPark mice, coupled with enhanced degeneration of DA neurons in the diabetic MitoPark mice. Ex vivo, in differentiated human DA neurons, IR was associated with increased SNCA and reactive oxygen species (ROS) levels, as well as mitochondrial depolarization. Moreover, we demonstrated concomitant hyperactivation of polo-like kinase-2 (PLK2), and upregulated p-SNCA (Ser129) and proteinase K-resistant SNCA proteins level in IR SH-SY5Y cells, however the inhibition of PLK2 reversed IR-related increases in phosphorylated and total SNCA. Similarly, the overexpression of peroxisome proliferator-activated receptor-γ coactivator 1-alpha (PGC)-1α suppressed ROS production, repressed PLK2 hyperactivity, and resulted in downregulation of total and Ser129-phosphorylated SNCA in the IR SH-SY5Y cells. Conclusions: These findings demonstrate that IR-associated diabetes promotes the development and progression of PD through PLK2-mediated mitochondrial dysfunction, upregulated ROS production, and enhanced SNCA signaling, suggesting the therapeutic targetability of PLK2 and/or SNCA as potential novel disease-modifying strategies in patients with PD.
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Marcellino, Daniel, Eva Lindqvist, Marion Schneider, Christa E. Müller, Kjell Fuxe, Lars Olson, and Dagmar Galter. "Chronic A2A antagonist treatment alleviates parkinsonian locomotor deficiency in MitoPark mice." Neurobiology of Disease 40, no. 2 (November 2010): 460–66. http://dx.doi.org/10.1016/j.nbd.2010.07.008.

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Cong, Linlin, Eric R. Muir, Cang Chen, Yusheng Qian, Jingwei Liu, K. C. Biju, Robert A. Clark, Senlin Li, and Timothy Q. Duong. "Multimodal MRI Evaluation of the MitoPark Mouse Model of Parkinson’s Disease." PLOS ONE 11, no. 3 (March 22, 2016): e0151884. http://dx.doi.org/10.1371/journal.pone.0151884.

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Hsieh, Tsung-Hsun, Chi-Wei Kuo, Kai-Hsuan Hsieh, Meng-Jyh Shieh, Chih-Wei Peng, Yen-Chien Chen, Ying-Ling Chang, et al. "Probiotics Alleviate the Progressive Deterioration of Motor Functions in a Mouse Model of Parkinson's Disease." Brain Sciences 10, no. 4 (April 1, 2020): 206. http://dx.doi.org/10.3390/brainsci10040206.

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Parkinson’s disease (PD) is one of the common long-term degenerative disorders that primarily affect motor systems. Gastrointestinal (GI) symptoms are common in individuals with PD and often present before motor symptoms. It has been found that gut dysbiosis to PD pathology is related to the severity of motor and non-motor symptoms in PD. Probiotics have been reported to have the ability to improve the symptoms related to constipation in PD patients. However, the evidence from preclinical or clinical research to verify the beneficial effects of probiotics for the motor functions in PD is still limited. An experimental PD animal model could be helpful in exploring the potential therapeutic strategy using probiotics. In the current study, we examined whether daily and long-term administration of probiotics has neuroprotective effects on nigrostriatal dopamine neurons and whether it can further alleviate the motor dysfunctions in PD mice. Transgenic MitoPark PD mice were chosen for this study and the effects of daily probiotic treatment on gait, beam balance, motor coordination, and the degeneration levels of dopaminergic neurons were identified. From the results, compared with the sham treatment group, we found that the daily administration of probiotics significantly reduced the motor impairments in gait pattern, balance function, and motor coordination. Immunohistochemically, a tyrosine hydroxylase (TH)-positive cell in the substantia nigra was significantly preserved in the probiotic-treated PD mice. These results showed that long-term administration of probiotics has neuroprotective effects on dopamine neurons and further attenuates the deterioration of motor dysfunctions in MitoPark PD mice. Our data further highlighted the promising possibility of the potential use of probiotics, which could be the relevant approach for further application on human PD subjects.
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Beckstead, Michael J., and Rebecca D. Howell. "Progressive parkinsonism due to mitochondrial impairment: Lessons from the MitoPark mouse model." Experimental Neurology 341 (July 2021): 113707. http://dx.doi.org/10.1016/j.expneurol.2021.113707.

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Ekstrand, M. I., F. Sterky Hansson, M. Terzioglu, L. Olson, and N. G. Larsson. "O.021 The MitoPark mouse - using mouse genetics to impair DA neuron mitochondria." Parkinsonism & Related Disorders 15 (December 2009): S7. http://dx.doi.org/10.1016/s1353-8020(09)70036-7.

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Gellhaar, S., D. Marcellino, M. B. Abrams, and D. Galter. "Chronic L‐ DOPA induces hyperactivity, normalization of gait and dyskinetic behavior in MitoPark mice." Genes, Brain and Behavior 14, no. 3 (March 2015): 260–70. http://dx.doi.org/10.1111/gbb.12210.

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Ghaisas, Shivani, Monica R. Langley, Bharathi N. Palanisamy, Somak Dutta, Kirthi Narayanaswamy, Paul J. Plummer, Souvarish Sarkar, et al. "MitoPark transgenic mouse model recapitulates the gastrointestinal dysfunction and gut-microbiome changes of Parkinson’s disease." NeuroToxicology 75 (December 2019): 186–99. http://dx.doi.org/10.1016/j.neuro.2019.09.004.

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Zhang, Y., A. C. Granholm, K. Huh, L. Shan, O. Diaz-Ruiz, N. Malik, L. Olson, et al. "PTEN deletion enhances survival, neurite outgrowth and function of dopamine neuron grafts to MitoPark mice." Brain 135, no. 9 (September 1, 2012): 2736–49. http://dx.doi.org/10.1093/brain/aws196.

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Farrand, Ariana Q., Rebecca A. Gregory, Cristina M. Bäckman, Kristi L. Helke, and Heather A. Boger. "Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease." Brain Research 1651 (November 2016): 88–94. http://dx.doi.org/10.1016/j.brainres.2016.09.025.

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Dissertations / Theses on the topic "MitoPark"

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Saraiva, Tatiana Margarida Lança. "Behaviour Phenotyping of Parkinson’s Disease Animal Models Using Inertial Sensors." Master's thesis, 2021. http://hdl.handle.net/10451/49401.

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Tese de mestrado Bioquímica (Bioquímica Médica) Universidade de Lisboa, Faculdade de Ciências, 2021
Parkinson’s Disease is a progressive degenerative illness of the human nervous system that affects basal ganglia circuits. It is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, loss of dopaminergic terminals in the striatum and widespread intracellular α-synuclein accumulation. Parkinson’s disease patients present three main motor symptoms: bradykinesia, muscular rigidity and tremor. Nevertheless, patients can also have additional motor and non-motor symptoms, such as apathy, depression, constipation, sleep behavior disorders, loss of sense of smell and cognitive impairment. At the time patients are first diagnosed, the loss of dopaminergic neurons in the substantia nigra pars compacta is already marked and the neurodegeneration has spread to other central nervous system regions. Nowadays, the most effective therapeutic strategy for Parkinson is the administration of Levodopa, a precursor of dopamine, that restores dopaminergic transmission in the nigrostriatal pathway. Nevertheless, Levodopa does not have an effect on the progression of the disease and its continuous administration induces the appearance of dyskinesias. These factors illustrate the importance of searching for novel ways of assessing these disease manifestations at early stages and why finding biomarkers that can reflect the disease progression would play an important role in clinical trials and in research using animal models, that are essential for the testing of new therapeutic approaches. As mentioned above, one way to study the degenerative process leading to Parkinson is using animal models. The MitoPark mice is an animal model for Parkinson Disease that mimics the progressive degeneration of the dopaminergic system through the knockout of the gene for mitochondrial transcription factor A (Tfam) in dopaminergic neurons using the Cre-loxP system. These mice lacking Tfam develop progressive respiratory chain deficiency followed by cell death. As a consequence of the progressive loss of dopaminergic neurons these mice develop Parkinson’s disease-like motor disabilities with ageing. In this project, we accessed both normal and Levodopa-induced behaviour of MitoPark mice using inertial sensors combined with video recordings. The use of inertial sensors allows the acquisition of high-resolution data, bringing the possibility of detecting behaviour patterns as the dopaminergic loss progresses that can be missed by the traditional simple video-tracking approach. Using these sensors we found a new biomarker to track the disease progression in this model that is based on the frequency domain of acceleration recordings. In addition to it, although the MitoPark mice responded to Levodopa with an increase in their acceleration and speed, the Levodopa treatment was not able to decrease the frequency domain of acceleration to control-like values. Altogether, our work shows that motion sensors are adequate for tracking disease progression and allow the measure of novel biomarkers, which may lead to a step further in the current endeavour of searching for novel therapeutic strategies for PD.
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Book chapters on the topic "MitoPark"

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"MitoPark." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1236. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_10553.

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