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Journal articles on the topic 'MitoPark'

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

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Chen, Yuan-Hao, Vicki Wang, Eagle Yi-Kung Huang, Yu-Ching Chou, Tung-Tai Kuo, Lars Olson, and Barry J. Hoffer. "Delayed Dopamine Dysfunction and Motor Deficits in Female Parkinson Model Mice." International Journal of Molecular Sciences 20, no. 24 (December 11, 2019): 6251. http://dx.doi.org/10.3390/ijms20246251.

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This study analyzed gender differences in the progressive dopamine (DA) deficiency phenotype in the MitoPark (MP) mouse model of Parkinson’s disease (PD) with progressive loss of DA release and reuptake in midbrain DA pathways. We found that the progressive loss of these DA presynaptic parameters begins significantly earlier in male than female MP mice. This was correlated with behavioral gender differences of both forced and spontaneous motor behavior. The degeneration of the nigrostriatal DA system in MP mice is earlier and more marked than that of the mesolimbic DA system, with male MP mice again being more strongly affected than female MP mice. After ovariectomy, DA presynaptic and behavioral changes in female mice become very similar to those of male animals. Our results suggest that estrogen, either directly or indirectly, is neuroprotective in the midbrain DA system. Our results are compatible with epidemiological data on incidence and symptom progression in PD, showing that men are more strongly affected than women at early ages.
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12

Langley, Monica, Anamitra Ghosh, Adhithiya Charli, Souvarish Sarkar, Muhammet Ay, Jie Luo, Jacek Zielonka, et al. "Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice." Antioxidants & Redox Signaling 27, no. 14 (November 10, 2017): 1048–66. http://dx.doi.org/10.1089/ars.2016.6905.

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13

Li, Xiuhua, Laney Redus, Cang Chen, Paul A. Martinez, Randy Strong, Senlin Li, and Jason C. O’Connor. "Cognitive Dysfunction Precedes the Onset of Motor Symptoms in the MitoPark Mouse Model of Parkinson’s Disease." PLoS ONE 8, no. 8 (August 15, 2013): e71341. http://dx.doi.org/10.1371/journal.pone.0071341.

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14

Galter, D., K. Pernold, T. Yoshitake, E. Lindqvist, B. Hoffer, J. Kehr, N. G. Larsson, and L. Olson. "MitoPark mice mirror the slow progression of key symptoms and L-DOPA response in Parkinson's disease." Genes, Brain and Behavior 9, no. 2 (March 2010): 173–81. http://dx.doi.org/10.1111/j.1601-183x.2009.00542.x.

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15

Clement, Amalie, Cathy Mitchelmore, Daniel Andersson, and Ayodeji A. Asuni. "P2-103: Altered Expression Levels of Neurofilaments in Brain and CSF in TG4510 and Mitopark MICE." Alzheimer's & Dementia 12 (July 2016): P651. http://dx.doi.org/10.1016/j.jalz.2016.06.1309.

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16

Clement, Amalie, Cathy Mitchelmore, Daniel R. Andersson, and Ayodeji A. Asuni. "Cerebrospinal fluid neurofilament light chain as a biomarker of neurodegeneration in the Tg4510 and MitoPark mouse models." Neuroscience 354 (June 2017): 101–9. http://dx.doi.org/10.1016/j.neuroscience.2017.04.030.

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17

Ekstrand, Mats I., and Dagmar Galter. "The MitoPark Mouse – An animal model of Parkinson's disease with impaired respiratory chain function in dopamine neurons." Parkinsonism & Related Disorders 15 (December 2009): S185—S188. http://dx.doi.org/10.1016/s1353-8020(09)70811-9.

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18

Smith, Karen M., Susan E. Browne, Srinivasan Jayaraman, Carina J. Bleickardt, Lisa M. Hodge, Edward Lis, Leon Yao, et al. "Effects of the selective adenosine A2A receptor antagonist, SCH 412348, on the parkinsonian phenotype of MitoPark mice." European Journal of Pharmacology 728 (April 2014): 31–38. http://dx.doi.org/10.1016/j.ejphar.2014.01.052.

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19

Branch, Sarah Y., Cang Chen, Ramaswamy Sharma, James D. Lechleiter, Senlin Li, and Michael J. Beckstead. "Dopaminergic Neurons Exhibit an Age-Dependent Decline in Electrophysiological Parameters in the MitoPark Mouse Model of Parkinson's Disease." Journal of Neuroscience 36, no. 14 (April 6, 2016): 4026–37. http://dx.doi.org/10.1523/jneurosci.1395-15.2016.

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20

Langley, Monica R., Shivani Ghaisas, Bharathi N. Palanisamy, Muhammet Ay, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, and Anumantha G. Kanthasamy. "Characterization of nonmotor behavioral impairments and their neurochemical mechanisms in the MitoPark mouse model of progressive neurodegeneration in Parkinson's disease." Experimental Neurology 341 (July 2021): 113716. http://dx.doi.org/10.1016/j.expneurol.2021.113716.

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21

Langley, Monica R., Shivani Ghaisas, Muhammet Ay, Jie Luo, Bharathi N. Palanisamy, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, and Anumantha G. Kanthasamy. "Manganese exposure exacerbates progressive motor deficits and neurodegeneration in the MitoPark mouse model of Parkinson’s disease: Relevance to gene and environment interactions in metal neurotoxicity." NeuroToxicology 64 (January 2018): 240–55. http://dx.doi.org/10.1016/j.neuro.2017.06.002.

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22

Ay, Muhammet, Jie Luo, Monica Langley, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, and Anumantha G. Kanthasamy. "Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease." Journal of Neurochemistry 141, no. 5 (May 9, 2017): 766–82. http://dx.doi.org/10.1111/jnc.14033.

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23

Grauer, Steven M., Robert Hodgson, and Lynn A. Hyde. "MitoPark mice, an animal model of Parkinson’s disease, show enhanced prepulse inhibition of acoustic startle and no loss of gating in response to the adenosine A2A antagonist SCH 412348." Psychopharmacology 231, no. 7 (October 23, 2013): 1325–37. http://dx.doi.org/10.1007/s00213-013-3320-5.

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24

Jones, Sarah, Cecile Martel, Anne-Sophie Belzacq-Casagrande, Catherine Brenner, and John Howl. "Mitoparan and target-selective chimeric analogues: Membrane translocation and intracellular redistribution induces mitochondrial apoptosis." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1783, no. 5 (May 2008): 849–63. http://dx.doi.org/10.1016/j.bbamcr.2008.01.009.

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25

Jones, Sarah, and John Howl. "Enantiomer-Specific Bioactivities of Peptidomimetic Analogues of Mastoparan and Mitoparan: Characterization of Inverso Mastoparan as a Highly Efficient Cell Penetrating Peptide." Bioconjugate Chemistry 23, no. 1 (January 9, 2012): 47–56. http://dx.doi.org/10.1021/bc2002924.

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26

Howl, John, Lewis Howl, and Sarah Jones. "The cationic tetradecapeptide mastoparan as a privileged structure for drug discovery: Enhanced antimicrobial properties of mitoparan analogues modified at position-14." Peptides 101 (March 2018): 95–105. http://dx.doi.org/10.1016/j.peptides.2018.01.007.

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27

"Chronic L-DOPA induces hyperactivity, normalization of gait and dyskinetic behavior in MitoPark mice." Genes, Brain and Behavior 14, no. 5 (April 29, 2015): 442. http://dx.doi.org/10.1111/gbb.12218.

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28

Chen, Cang, Xiuhua Li, Guo Ge, Jingwei Liu, K. C. Biju, Suzette D. Laing, Yusheng Qian, et al. "GDNF-expressing macrophages mitigate loss of dopamine neurons and improve Parkinsonian symptoms in MitoPark mice." Scientific Reports 8, no. 1 (April 3, 2018). http://dx.doi.org/10.1038/s41598-018-23795-4.

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29

"Mitopure™ (Proprietary Urolithin A) Bioavailability in Healthy Adults." Case Medical Research, November 13, 2019. http://dx.doi.org/10.31525/ct1-nct04160312.

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30

"Industry Watch." Asia-Pacific Biotech News 11, no. 16 (August 30, 2007): 1118–35. http://dx.doi.org/10.1142/s021903030700122x.

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Apollo Succeeds in Needle-Free Drug Delivery Trials. HealthLinx Enters New Trials for Ovarian Cancer Diagnostics. Sinovac and GlaxoSmithKline (China) Investment Co Enters Exclusive Promotion Service Agreement. Hong Kong University of Science and Technology to Award Exclusive License to MitoPharm. GVK Biosciences to Provide Clinical Biomarker Database to USFDA Genomics Group. Ranbaxy Commercializes its First Authorized Generic Product in the US. KineMed Inc Extends Alliance with CMIC. Kyowa Hakko Licenses BioWa Novel Antibody Engineering Technology. Japan's Bioventure Today — UMN Pharma Inc. Abott Picks Singapore for Trial of New Drug. A*STAR and NUS Establish New Clinical Imaging Research Center with Siemens.
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31

Richardson, Adam, Lewis Muir, Sasha Mousdell, Darren Sexton, Sarah Jones, John Howl, and Kehinde Ross. "Modulation of mitochondrial activity in HaCaT keratinocytes by the cell penetrating peptide Z-Gly-RGD(DPhe)-mitoparan." BMC Research Notes 11, no. 1 (January 30, 2018). http://dx.doi.org/10.1186/s13104-018-3192-1.

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