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Loss of autophagy in the central nervous system causes neurodegeneration in mice

Author

Listed:
  • Masaaki Komatsu

    (Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku
    Juntendo University School of Medicine, Bunkyo-ku)

  • Satoshi Waguri

    (Osaka University Graduate School of Medicine
    Fukushima Medical University School of Medicine)

  • Tomoki Chiba

    (Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku)

  • Shigeo Murata

    (Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku)

  • Jun-ichi Iwata

    (Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku
    Juntendo University School of Medicine, Bunkyo-ku)

  • Isei Tanida

    (Juntendo University School of Medicine, Bunkyo-ku)

  • Takashi Ueno

    (Juntendo University School of Medicine, Bunkyo-ku)

  • Masato Koike

    (Osaka University Graduate School of Medicine)

  • Yasuo Uchiyama

    (Osaka University Graduate School of Medicine)

  • Eiki Kominami

    (Juntendo University School of Medicine, Bunkyo-ku)

  • Keiji Tanaka

    (Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku)

Abstract

A tidy cell is a healthy cell Two papers this week suggest that the process of protein degradation and clearance of cellular components may be more important in maintaining the health of the nervous system than was thought. Both groups show that inhibition of autophagy in mouse brain cells results in neurodegeneration and early death. Autophagy, the protein degradation and recycling of cellular components, is important for the normal growth and development of a cell. The finding that the continual clearance of cellular components is essential for maintaining neuronal health should open up new avenues of research into the nature of neurodegenerative diseases.

Suggested Citation

  • Masaaki Komatsu & Satoshi Waguri & Tomoki Chiba & Shigeo Murata & Jun-ichi Iwata & Isei Tanida & Takashi Ueno & Masato Koike & Yasuo Uchiyama & Eiki Kominami & Keiji Tanaka, 2006. "Loss of autophagy in the central nervous system causes neurodegeneration in mice," Nature, Nature, vol. 441(7095), pages 880-884, June.
  • Handle: RePEc:nat:nature:v:441:y:2006:i:7095:d:10.1038_nature04723
    DOI: 10.1038/nature04723
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    Cited by:

    1. Afshin Saffari & Barbara Brechmann & Cedric Böger & Wardiya Afshar Saber & Hellen Jumo & Dosh Whye & Delaney Wood & Lara Wahlster & Julian E. Alecu & Marvin Ziegler & Marlene Scheffold & Kellen Winden, 2024. "High-content screening identifies a small molecule that restores AP-4-dependent protein trafficking in neuronal models of AP-4-associated hereditary spastic paraplegia," Nature Communications, Nature, vol. 15(1), pages 1-22, December.
    2. Catherine J. Greene & Jenny A. Nguyen & Samuel M. Cheung & Corey R. Arnold & Dale R. Balce & Ya Ting Wang & Adrian Soderholm & Neil McKenna & Devin Aggarwal & Rhiannon I. Campden & Benjamin W. Ewanchu, 2022. "Macrophages disseminate pathogen associated molecular patterns through the direct extracellular release of the soluble content of their phagolysosomes," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    3. Xiaoting Zhou & You-Kyung Lee & Xianting Li & Henry Kim & Carlos Sanchez-Priego & Xian Han & Haiyan Tan & Suiping Zhou & Yingxue Fu & Kerry Purtell & Qian Wang & Gay R. Holstein & Beisha Tang & Junmin, 2024. "Integrated proteomics reveals autophagy landscape and an autophagy receptor controlling PKA-RI complex homeostasis in neurons," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    4. Barbara Baldo & Rana Soylu & Åsa Petersén, 2013. "Maintenance of Basal Levels of Autophagy in Huntington’s Disease Mouse Models Displaying Metabolic Dysfunction," PLOS ONE, Public Library of Science, vol. 8(12), pages 1-15, December.
    5. Alexandra K. Davies & Julian E. Alecu & Marvin Ziegler & Catherine G. Vasilopoulou & Fabrizio Merciai & Hellen Jumo & Wardiya Afshar-Saber & Mustafa Sahin & Darius Ebrahimi-Fakhari & Georg H. H. Borne, 2022. "AP-4-mediated axonal transport controls endocannabinoid production in neurons," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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