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<article article-type="review-article" dtd-version="1.1" xml:lang="en" xmlns:xlink="http://www.w3.org/1999/xlink"><front><journal-meta><journal-id journal-id-type="publisher-id">NRO</journal-id><journal-id journal-id-type="nlm-ta">Neuroscientist</journal-id><journal-title-group><journal-title>The Neuroscientist</journal-title></journal-title-group><issn pub-type="ppub">1073-8584</issn><issn pub-type="epub">1089-4098</issn><publisher><publisher-name>SAGE Publications</publisher-name><publisher-loc>Sage CA: Los Angeles, CA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1177/10738584251324459</article-id><article-id pub-id-type="publisher-id">10.1177_10738584251324459</article-id><article-categories><subj-group subj-group-type="heading"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>How does autophagy impact neurological function?</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Fleming</surname><given-names>Angeleen</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff2-10738584251324459">2</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><name><surname>Lopez</surname><given-names>Ana</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff2-10738584251324459">2</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><name><surname>Rob</surname><given-names>Matea</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><name><surname>Ramakrishna</surname><given-names>Sarayu</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>So Jung</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Xinyi</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-5002-5263</contrib-id><name><surname>Rubinsztein</surname><given-names>David C.</given-names></name><xref ref-type="aff" rid="aff1-10738584251324459">1</xref><xref ref-type="aff" rid="aff3-10738584251324459">3</xref><xref ref-type="corresp" rid="corresp1-10738584251324459"/></contrib></contrib-group><aff id="aff1-10738584251324459"><label>1</label>Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Cambridge, UK</aff><aff id="aff2-10738584251324459"><label>2</label>Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK</aff><aff id="aff3-10738584251324459"><label>3</label>UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, Cambridge, UK</aff><author-notes><corresp id="corresp1-10738584251324459">David C. Rubinsztein, Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK. Email: <email>dcr1000@cam.ac.uk</email></corresp></author-notes><pub-date pub-type="epub"><day>13</day><month>3</month><year>2025</year></pub-date><volume>31</volume><issue>4</issue><fpage>349</fpage><lpage>364</lpage><permissions><copyright-statement>© The Author(s) 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder content-type="sage">SAGE Publications</copyright-holder><license><ali:license_ref start_date="2025-03-13" xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0/</ali:license_ref><license-p>This article is distributed under the terms of the Creative Commons Attribution 4.0 License (<ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by/4.0/">https://creativecommons.org/licenses/by/4.0/</ext-link>) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (<ext-link ext-link-type="uri" xlink:href="https://us.sagepub.com/en-us/nam/open-access-at-sage">https://us.sagepub.com/en-us/nam/open-access-at-sage</ext-link>).</license-p></license></permissions><abstract><p>Autophagies describe a set of processes in which cells degrade their cytoplasmic contents via various routes that terminate with the lysosome. In macroautophagy (the focus of this review, henceforth autophagy), cytoplasmic contents, including misfolded proteins, protein complexes, dysfunctional organelles, and various pathogens, are captured within double membranes called autophagosomes, which ultimately fuse with lysosomes, after which their contents are degraded. Autophagy is important in maintaining neuronal and glial function; consequently, disrupted autophagy is associated with various neurologic diseases. This review provides a broad perspective on the roles of autophagy in the CNS, highlighting recent literature that furthers our understanding of the multifaceted role of autophagy in maintaining a healthy nervous system.</p></abstract><kwd-group><kwd>autophagy</kwd><kwd>neuron</kwd><kwd>neural stem cell</kwd><kwd>aggregates</kwd><kwd>neuroinflammation</kwd><kwd>glia</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>typesetter</meta-name><meta-value>ts1</meta-value></custom-meta></custom-meta-group></article-meta></front></article>