Mechanisms underlying neuronal dysfunction and degeneration caused by loss of presynaptic mitochondria
Project/Area Number |
15K06712
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurophysiology / General neuroscience
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Research Institution | Tokyo Metropolitan University |
Principal Investigator |
Ando Kanae 首都大学東京, 理工学研究科, 准教授 (40632500)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | ミトコンドリア / 神経細胞死 / 加齢 / 軸索輸送 / エネルギー代謝 / 神経変性疾患 / CaMKII / 神経細胞 / 細胞内局在 / ATP / 軸索 / 遺伝子発現 |
Outline of Final Research Achievements |
Brain nerve cells extend long processes to communicate with other cells. The contact sites are called synapses and demand energy supply to function. To meet the energy demands, mitochondria, tiny powerhouses in the cell, are transported from the cell body of the nerve cells. Depletion of mitochondria from the cells disrupts neuronal functions and eventually causes neuronal death. However, how the loss of synaptic mitochondria leads to neuronal death is not known. To elucidate the underlying molecular mechanisms, we used transgenic fruit fly to deplete mitochondria from synapses. We identified several molecules that are involved in neuronal dysfunction and cell loss triggered by loss of synaptic mitochondria. Since the loss of synaptic mitochondria is associated with neurodegenerative diseases such as Alzheimer’s disease, these findings may lead to development of a cure.
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Report
(4 results)
Research Products
(23 results)
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[Journal Article] Stabilization of microtubule-unbound tau via tau phosphorylation at Ser262/356 by Par-1/MARK contributes to augmentation of AD-related phosphorylation and Aβ42-induced tau toxicity.2016
Author(s)
Ando, K.*, Maruko-Otake, A., Ohtake, Y., Hayashishita, M., Sekiya, M., and Iijima, K. M.
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Journal Title
PLoS Genetics
Volume: 12(3)
Issue: 3
Pages: e1005917-e1005917
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Presentation] CaMKII enhances tau-mediated neurodegeneration downstream of tau phosphorylation in transgenic Drosophila models of tauopathy.2017
Author(s)
Ando*, K., Oka, M., Maruko-Otake, A., Ohtake, Y., Sekiya, M., Hisanaga, S., Iijima, K.M.
Organizer
The 4th Asia-Pacific Drosophila Research Conference, Suita, Osaka, Japan, May 10, 2017.
Related Report
Int'l Joint Research
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[Presentation] “Reduction in ATP levels in the axon during aging and the role of mitochondrial distribution.” (selected for oral presentation at nano symposium)2016
Author(s)
Oka,M., Suzuki, E., Hisanaga, S., Iijima, KM, and Ando., K.
Organizer
46th annual meeting of Society for Neuroscience
Place of Presentation
San Diego, USA
Related Report
Int'l Joint Research
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[Presentation] Sustained activation of CaMKII caused by depletion of mitochondria from the axon enhances tau toxicity. (selected for oral presentation at nano symposium)2016
Author(s)
Ando, K., Maruko-Otake, A., Hayashishita, M., Oka, M., Ohtake, Y., Sekiya, M., Saito, T., Hisanaga, S., and Iijima, KM.
Organizer
46th annual meeting of Society for Neuroscience
Place of Presentation
San Diego, USA
Related Report
Int'l Joint Research
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[Presentation] “Pathological stabilization of tau through phosphorylation at Ser262/356 by Par-1/MARK contributes to abnormal metabolism and toxicity of tau caused by Aβ42”2015
Author(s)
Ando, K.*, Maruko-Otake, A., Ohtake, Y., Hayashishita, M., Sekiya, M. and Iijima, K. M.Nagoya, Japan
Organizer
The 1st Internatinal Symposium of “Brain Protein Aging and Dementia Control”,
Place of Presentation
名古屋
Year and Date
2015-10-09
Related Report
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[Presentation] “Tau phosphorylation via microtubule affinity regulating kinase MARK/PAR1 as an initial step in the pathological cascade leading to neurodegeneration”2015
Author(s)
Ando, K. *, Hayashishita, M., Oka,M., Maruko-Otake, A., Ohtake, Y., Iijima, K.M.
Organizer
The 58th Annual Meeting of the Japanese Society for Neurochemistry
Place of Presentation
埼玉
Year and Date
2015-09-11
Related Report
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[Book] Neuromethods, Chapter: Electron microscopy of the brains of Drosophila Models of Alzheimer’s disease. DOI 10.1007/7657_2015_75,2016
Author(s)
Ando, K.*, Hearn, A., Suzuki, E., Maruko-Otake, A., Sekiya, M., and Iijima, K.M.
Total Pages
19
Publisher
Springer
Related Report