Temat: "Cell death in the nervous system" - OpacWWW

Skocz do pozycji: 1.

Tytuł:: Light-driven activation of mitochondrial proton-motive force improves motor behaviors in a Drosophila model of Parkinson's disease.
Autorzy:: Imai Y; 1Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.; 2Department of Neurology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.
Inoshita T; 3Department of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.
Meng H; 4Department of Neurodegenerative and Demented Disorders, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.
Shiba-Fukushima K; 3Department of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.
Hara KY; 5Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, 422-8526 Japan.
Sawamura N; 6Research Organization for Nano & Life Innovation, Waseda University, Tokyo, 162-8480 Japan.; 7Faculty of Science and Engineering, Waseda University, Tokyo, 162-8480 Japan.
Hattori N; 1Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.; 2Department of Neurology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.; 3Department of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.; 4Department of Neurodegenerative and Demented Disorders, Juntendo University Graduate School of Medicine, Tokyo, 113-8421 Japan.; Pokaż więcej
Źródło:: Communications biology [Commun Biol] 2019 Nov 22; Vol. 2, pp. 424. Date of Electronic Publication: 2019 Nov 22 (Print Publication: 2019).
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:: Light*
Motor Activity*
Protons*
Mitochondria/*metabolism
Mitochondria/*radiation effects
Mitochondrial Diseases/*etiology
Mitochondrial Diseases/*metabolism
Parkinson Disease/*etiology
Parkinson Disease/*metabolism
Animals ; Biomarkers ; Disease Models, Animal ; Disease Susceptibility ; Dopaminergic Neurons/metabolism ; Drosophila ; Models, Biological ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; alpha-Synuclein/metabolism
SCR Disease Name:: Parkinson Disease, Mitochondrial

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Skocz do pozycji: 2.

Tytuł:: Inhibition of the glutamine transporter SNAT1 confers neuroprotection in mice by modulating the mTOR-autophagy system.
Autorzy:: Yamada D; 1Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Kawabe K; 1Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Tosa I; 1Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Tsukamoto S; 1Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Nakazato R; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Kou M; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Fujikawa K; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Nakamura S; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Ono M; 3Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Oohashi T; 3Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.
Kaneko M; 4Laboratory for Animal Resource Development Unit and Genetic Engineering Team, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan.
Go S; 4Laboratory for Animal Resource Development Unit and Genetic Engineering Team, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima Minami, Chuou-ku, Kobe, Hyogo 650-0047 Japan.
Hinoi E; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Yoneda Y; 2Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Graduate School, Kanazawa, Ishikawa 920-1192 Japan.
Takarada T; 1Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8558 Japan.; Pokaż więcej
Źródło:: Communications biology [Commun Biol] 2019 Sep 18; Vol. 2, pp. 346. Date of Electronic Publication: 2019 Sep 18 (Print Publication: 2019).
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:: Amino Acid Transport System A/*antagonists & inhibitors
Amino Acid Transport System A/*metabolism
Autophagy/*drug effects
Neuroprotective Agents/*pharmacology
TOR Serine-Threonine Kinases/*metabolism
Amino Acid Transport System A/genetics ; Animals ; Cerebral Infarction/etiology ; Cerebral Infarction/metabolism ; Cerebral Infarction/pathology ; Gene Expression ; Genetic Loci ; Genome ; Immunohistochemistry ; Mice ; Mice, Knockout ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotection ; Organ Specificity

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