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Bus C, Zizmare L, Feldkaemper M, et al. Human Dopaminergic Neurons Lacking PINK1 Exhibit Disrupted Dopamine Metabolism Related to Vitamin B6 Co-Factors. iScience. 2020;23(12):101797doi: 10.1016/j.isci.2020.101797.
Bus, C., Zizmare, L., Feldkaemper, M., Geisler, S., Zarani, M., Schaedler, A., Klose, F., Admard, J., Mageean, C. J., Arena, G., Fallier-Becker, P., Ugun-Klusek, A., Maruszczak, K. K., Kapolou, K., Schmid, B., Rapaport, D., Ueffing, M., Casadei, N., Krüger, R., Gasser, T., Vogt Weisenhorn, D. M., Kahle, P. J., Trautwein, C., Gloeckner, C. J., & Fitzgerald, J. C. (2020). Human Dopaminergic Neurons Lacking PINK1 Exhibit Disrupted Dopamine Metabolism Related to Vitamin B6 Co-Factors. iScience, 23(12), 101797. https://doi.org/10.1016/j.isci.2020.101797
Bus, Christine, et al. "Human Dopaminergic Neurons Lacking PINK1 Exhibit Disrupted Dopamine Metabolism Related to Vitamin B6 Co-Factors." iScience vol. 23,12 (2020): 101797. doi: https://doi.org/10.1016/j.isci.2020.101797
Bus C, Zizmare L, Feldkaemper M, Geisler S, Zarani M, Schaedler A, Klose F, Admard J, Mageean CJ, Arena G, Fallier-Becker P, Ugun-Klusek A, Maruszczak KK, Kapolou K, Schmid B, Rapaport D, Ueffing M, Casadei N, Krüger R, Gasser T, Vogt Weisenhorn DM, Kahle PJ, Trautwein C, Gloeckner CJ, Fitzgerald JC. Human Dopaminergic Neurons Lacking PINK1 Exhibit Disrupted Dopamine Metabolism Related to Vitamin B6 Co-Factors. iScience. 2020 Nov 13;23(12):101797. doi: 10.1016/j.isci.2020.101797. eCollection 2020 Dec 18. PMID: 33299968; PMCID: PMC7702004.
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iScience. 2020 Nov 13;23(12):101797. doi: 10.1016/j.isci.2020.101797. eCollection 2020 Dec 18.

Human Dopaminergic Neurons Lacking PINK1 Exhibit Disrupted Dopamine Metabolism Related to Vitamin B6 Co-Factors.

iScience

Christine Bus, Laimdota Zizmare, Marita Feldkaemper, Sven Geisler, Maria Zarani, Anna Schaedler, Franziska Klose, Jakob Admard, Craig J Mageean, Giuseppe Arena, Petra Fallier-Becker, Aslihan Ugun-Klusek, Klaudia K Maruszczak, Konstantina Kapolou, Benjamin Schmid, Doron Rapaport, Marius Ueffing, Nicolas Casadei, Rejko Krüger, Thomas Gasser, Daniela M Vogt Weisenhorn, Philipp J Kahle, Christoph Trautwein, Christian J Gloeckner, Julia C Fitzgerald

Affiliations

  1. Department of Neurodegenerative Diseases, Centre of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Otfried Müller Strasse 27, 72076, Tübingen, Germany.
  2. DZNE - German Center for Neurodegenerative Diseases, Tübingen, Germany.
  3. Werner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, University of Tübingen, Tübingen, Germany.
  4. Institute for Ophthalmic Research, Centre for Ophthalmology, University of Tübingen, Tübingen, Germany.
  5. Graduate School of Cellular and Molecular Neuroscience, University of Tübingen, Tübingen, Germany.
  6. Core Facility for Medical Bioanalytics, University of Tübingen, Center for Ophthalmology, Institute for Ophthalmic Research, Tübingen, Germany.
  7. NGS Competence Center Tübingen, Institute of Medical Genetics and Applied Genomics, University of Tübingen, Germany.
  8. Translational Neuroscience, Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Luxembourg.
  9. Institute of Pathology and Neuropathology, University of Tübingen, Tübingen, Germany.
  10. School of Science and Technology, Nottingham Trent University, Nottingham, UK.
  11. Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany.
  12. Transversal Translational Medicine, Luxembourg Institute of Health (LIH), Strassen, Luxembourg.
  13. Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Developmental Genetics, Munich-Neuherberg, Germany.

PMID: 33299968 PMCID: PMC7702004 DOI: 10.1016/j.isci.2020.101797

Abstract

PINK1 loss-of-function mutations cause early onset Parkinson disease. PINK1-Parkin mediated mitophagy has been well studied, but the relevance of the endogenous process in the brain is debated. Here, the absence of PINK1 in human dopaminergic neurons inhibits ionophore-induced mitophagy and reduces mitochondrial membrane potential. Compensatory, mitochondrial renewal maintains mitochondrial morphology and protects the respiratory chain. This is paralleled by metabolic changes, including inhibition of the TCA cycle enzyme

© 2020 The Authors.

Keywords: Molecular Biology; Molecular Neuroscience; Omics; Stem Cells Research

Conflict of interest statement

The authors declare no conflict of interest.

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