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Reversible suppression of autophagy in a mouse model reveals neuronal resilience.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Reversible suppression of autophagy in a mouse model reveals neuronal resilience.
Συγγραφείς: Eguchi T; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan., Abe M; Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.; Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan., Tomita T; Division of Protein Metabolism, Institute of Medical Science, The University of Tokyo, Tokyo, Japan., Morishita H; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan., Saeki Y; Division of Protein Metabolism, Institute of Medical Science, The University of Tokyo, Tokyo, Japan., Sakimura K; Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan., Tanaka KF; Division of Brain Sciences, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan., Mizushima N; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.; International Research Center for Neurointelligence (WPI-IRCN), The University of Tokyo, Institutes for Advanced Study (UTIAS), The University of Tokyo, Tokyo, Japan.
Πηγή: Science (New York, N.Y.) [Science] 2026 Jun 25; Vol. 392 (6805), pp. 1363-1368. Date of Electronic Publication: 2026 Jun 25.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 0404511 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-9203 (Electronic) Linking ISSN: 00368075 NLM ISO Abbreviation: Science Subsets: MEDLINE
Imprint Name(s): Publication: : Washington, DC : American Association for the Advancement of Science
Original Publication: New York, N.Y. : [s.n.] 1880-
Ιατρικοί όροι (MeSH): Autophagy*/genetics , Autophagy*/drug effects , Neurons*/drug effects , Neurons*/pathology , Neurodegenerative Diseases*/pathology, Axons/pathology ; Animals ; Mice ; Disease Models, Animal ; Proteome ; Transcriptome ; Male ; Female ; Mice, Mutant Strains
Περίληψη: Impairments in intracellular quality-control mechanisms, including autophagy, affect neuronal integrity and function. Despite numerous studies aimed at slowing neuronal deterioration, it remains unclear whether neuronal function and intracellular quality can be restored once impaired. We developed a mouse model in which autophagy could be rapidly and reversibly regulated to investigate the reversibility of such defects. Suppressing autophagy led to proteome and transcriptome changes, inclusion body accumulation, and axonal swelling, all of which were largely ameliorated after autophagy restoration. Consistent with these cellular abnormalities, autophagy suppression induced motor and cognitive dysfunction, which was also reversed on autophagy restoration. Our findings elucidate the potential resilience of neuronal function and quality enabled by intracellular clearance.
Substance Nomenclature: 0 (Proteome)
Entry Date(s): Date Created: 20260625 Date Completed: 20260625 Latest Revision: 20260706
Update Code: 20260707
DOI: 10.1126/science.ady3911
PMID: 42348689
Βάση Δεδομένων: MEDLINE
FullText Text:
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PubType: Academic Journal
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  Data: Reversible suppression of autophagy in a mouse model reveals neuronal resilience.
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  Data: <searchLink fieldCode="AU" term="%22Eguchi+T%22">Eguchi T</searchLink>; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.<br /><searchLink fieldCode="AU" term="%22Abe+M%22">Abe M</searchLink>; Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.; Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.<br /><searchLink fieldCode="AU" term="%22Tomita+T%22">Tomita T</searchLink>; Division of Protein Metabolism, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.<br /><searchLink fieldCode="AU" term="%22Morishita+H%22">Morishita H</searchLink>; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.<br /><searchLink fieldCode="AU" term="%22Saeki+Y%22">Saeki Y</searchLink>; Division of Protein Metabolism, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.<br /><searchLink fieldCode="AU" term="%22Sakimura+K%22">Sakimura K</searchLink>; Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.<br /><searchLink fieldCode="AU" term="%22Tanaka+KF%22">Tanaka KF</searchLink>; Division of Brain Sciences, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.<br /><searchLink fieldCode="AU" term="%22Mizushima+N%22">Mizushima N</searchLink>; Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.; International Research Center for Neurointelligence (WPI-IRCN), The University of Tokyo, Institutes for Advanced Study (UTIAS), The University of Tokyo, Tokyo, Japan.
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  Data: <searchLink fieldCode="JN" term="%220404511%22">Science (New York, N.Y.)</searchLink> [Science] 2026 Jun 25; Vol. 392 (6805), pp. 1363-1368. <i>Date of Electronic Publication: </i>2026 Jun 25.
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  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22American+Association+for+the+Advancement+of+Science%22">American Association for the Advancement of Science </searchLink><i>Country of Publication: </i>United States <i>NLM ID: </i>0404511 <i>Publication Model: </i>Print-Electronic <i>Cited Medium: </i>Internet <i>ISSN: </i>1095-9203 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2200368075%22">00368075 </searchLink><i>NLM ISO Abbreviation: </i>Science <i>Subsets: </i>MEDLINE
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  Data: <i>Publication</i>: <Oct. 4, 1991- > : Washington, DC : American Association for the Advancement of Science<br /><i>Original Publication</i>: New York, N.Y. : [s.n.] 1880-
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  Data: <searchLink fieldCode="MM" term="%22Autophagy%22">Autophagy*</searchLink>/<searchLink fieldCode="MM" term="%22Autophagy+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Autophagy%22">Autophagy*</searchLink>/<searchLink fieldCode="MM" term="%22Autophagy+drug+effects%22">drug effects</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurons%22">Neurons*</searchLink>/<searchLink fieldCode="MM" term="%22Neurons+drug+effects%22">drug effects</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurons%22">Neurons*</searchLink>/<searchLink fieldCode="MM" term="%22Neurons+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases%22">Neurodegenerative Diseases*</searchLink>/<searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases+pathology%22">pathology</searchLink><br /><searchLink fieldCode="MH" term="%22Axons%22">Axons</searchLink>/<searchLink fieldCode="MH" term="%22Axons+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%22">Mice</searchLink> ; <searchLink fieldCode="MH" term="%22Disease+Models%2C+Animal%22">Disease Models, Animal</searchLink> ; <searchLink fieldCode="MH" term="%22Proteome%22">Proteome</searchLink> ; <searchLink fieldCode="MH" term="%22Transcriptome%22">Transcriptome</searchLink> ; <searchLink fieldCode="MH" term="%22Male%22">Male</searchLink> ; <searchLink fieldCode="MH" term="%22Female%22">Female</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%2C+Mutant+Strains%22">Mice, Mutant Strains</searchLink>
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  Label: Abstract
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  Data: Impairments in intracellular quality-control mechanisms, including autophagy, affect neuronal integrity and function. Despite numerous studies aimed at slowing neuronal deterioration, it remains unclear whether neuronal function and intracellular quality can be restored once impaired. We developed a mouse model in which autophagy could be rapidly and reversibly regulated to investigate the reversibility of such defects. Suppressing autophagy led to proteome and transcriptome changes, inclusion body accumulation, and axonal swelling, all of which were largely ameliorated after autophagy restoration. Consistent with these cellular abnormalities, autophagy suppression induced motor and cognitive dysfunction, which was also reversed on autophagy restoration. Our findings elucidate the potential resilience of neuronal function and quality enabled by intracellular clearance.
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  Data: <i>Date Created: </i>20260625 <i>Date Completed: </i>20260625 <i>Latest Revision: </i>20260706
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  Data: 10.1126/science.ady3911
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        Text: English
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        StartPage: 1363
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      – TitleFull: Reversible suppression of autophagy in a mouse model reveals neuronal resilience.
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              Text: 2026 Jun 25
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