Marc S. Lavine, Jesse Smith, Keith T. Smith, Phil Szuromi, Madeleine Seale, Sacha Vignieri, Melissa L. Norton, John Foley, Bianca Lopez, Mattia Maroso, Di Jiang, Yevgeniya Nusinovich, Sarah H. Ross, Michael A. Funk, Jake S. Yeston, Leoma Bere
{"title":"In Science Journals","authors":"Marc S. Lavine, Jesse Smith, Keith T. Smith, Phil Szuromi, Madeleine Seale, Sacha Vignieri, Melissa L. Norton, John Foley, Bianca Lopez, Mattia Maroso, Di Jiang, Yevgeniya Nusinovich, Sarah H. Ross, Michael A. Funk, Jake S. Yeston, Leoma Bere","doi":"10.1126/science.aeg3196","DOIUrl":"10.1126/science.aeg3196","url":null,"abstract":"","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kishalay De, Morgan MacLeod, Jacob E. Jencson, Elizabeth Lovegrove, Andrea Antoni, Erin Kara, Mansi M. Kasliwal, Ryan M. Lau, Abraham Loeb, Megan Masterson, Aaron M. Meisner, Christos Panagiotou, Eliot Quataert, Robert Simcoe
When a massive star reaches the end of its lifetime, its core collapses and releases neutrinos that drive a shock into the outer layers (the stellar envelope). A sufficiently strong shock ejects the envelope, producing a supernova. If the shock fails to eject it, the envelope is predicted to fall back onto the collapsing core, producing a stellar-mass black hole (BH) and causing the star to disappear. We report observations of M31-2014-DS1, a hydrogen-depleted supergiant in the Andromeda Galaxy. In 2014, it brightened in the mid-infrared, then from 2017 to 2022, it faded by factors of in optical light (becoming undetectable) and in total light. We interpret these observations, and those of a previous event in NGC 6946, as evidence for failed supernovae forming stellar-mass BHs.
{"title":"Disappearance of a massive star in the Andromeda Galaxy due to formation of a black hole","authors":"Kishalay De, Morgan MacLeod, Jacob E. Jencson, Elizabeth Lovegrove, Andrea Antoni, Erin Kara, Mansi M. Kasliwal, Ryan M. Lau, Abraham Loeb, Megan Masterson, Aaron M. Meisner, Christos Panagiotou, Eliot Quataert, Robert Simcoe","doi":"10.1126/science.adt4853","DOIUrl":"10.1126/science.adt4853","url":null,"abstract":"<div >When a massive star reaches the end of its lifetime, its core collapses and releases neutrinos that drive a shock into the outer layers (the stellar envelope). A sufficiently strong shock ejects the envelope, producing a supernova. If the shock fails to eject it, the envelope is predicted to fall back onto the collapsing core, producing a stellar-mass black hole (BH) and causing the star to disappear. We report observations of M31-2014-DS1, a hydrogen-depleted supergiant in the Andromeda Galaxy. In 2014, it brightened in the mid-infrared, then from 2017 to 2022, it faded by factors of <span><math><mrow><mo>≳</mo><msup><mrow><mn>10</mn></mrow><mn>4</mn></msup></mrow></math></span> in optical light (becoming undetectable) and <span><math><mrow><mo>≳</mo><mn>10</mn></mrow></math></span> in total light. We interpret these observations, and those of a previous event in NGC 6946, as evidence for failed supernovae forming stellar-mass BHs.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Josephine Elena Reek, Constantin M. Zohner, Gabriel Reuben Smith, Susan C. Cook-Patton, Pieter De Frenne, Paolo D’Odorico, Marius G. Floriancic, Robert B. Jackson, Julia A. Jones, James W. Kirchner, Marysa Laguë, Yuting Liang, Yuta J. Masuda, Robert I. McDonald, Luke A. Parsons, Benedict S. Probst, June T. Spector, Thales A. P. West, Nicholas H. Wolff, Florian Zellweger, Thomas W. Crowther
Forests regulate global and local climates in ways that impact human well-being. In this Review, we discuss the scale-dependent mechanisms through which forests regulate climate, highlighting their contributions to global mitigation and local adaptation. Locally, forests tend to buffer temperatures, cooling in warm conditions and warming in cold ones. In regions that naturally support dense forest cover, trees contribute to global cooling primarily through carbon uptake, with some offsetting from albedo-related warming. By enhancing rainfall interception, evapotranspiration, and cloud formation, forests also influence the hydrological cycle, lowering flood risks in humid regions but often reducing downstream water availability, especially in drier climates. Collectively, these interacting processes show that the greatest climate benefits occur where forests are native, highlighting their importance for both climate adaptation and mitigation.
{"title":"More than mitigation: The role of forests in climate adaptation","authors":"Josephine Elena Reek, Constantin M. Zohner, Gabriel Reuben Smith, Susan C. Cook-Patton, Pieter De Frenne, Paolo D’Odorico, Marius G. Floriancic, Robert B. Jackson, Julia A. Jones, James W. Kirchner, Marysa Laguë, Yuting Liang, Yuta J. Masuda, Robert I. McDonald, Luke A. Parsons, Benedict S. Probst, June T. Spector, Thales A. P. West, Nicholas H. Wolff, Florian Zellweger, Thomas W. Crowther","doi":"10.1126/science.ads4361","DOIUrl":"10.1126/science.ads4361","url":null,"abstract":"<div >Forests regulate global and local climates in ways that impact human well-being. In this Review, we discuss the scale-dependent mechanisms through which forests regulate climate, highlighting their contributions to global mitigation and local adaptation. Locally, forests tend to buffer temperatures, cooling in warm conditions and warming in cold ones. In regions that naturally support dense forest cover, trees contribute to global cooling primarily through carbon uptake, with some offsetting from albedo-related warming. By enhancing rainfall interception, evapotranspiration, and cloud formation, forests also influence the hydrological cycle, lowering flood risks in humid regions but often reducing downstream water availability, especially in drier climates. Collectively, these interacting processes show that the greatest climate benefits occur where forests are native, highlighting their importance for both climate adaptation and mitigation.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jared W. Westbrook, Joanna Malukiewicz, Qian Zhang, Avinash Sreedasyam, Jerry W. Jenkins, Vasiliy Lakoba, Sara Fitzsimmons, Jamie Van Clief, Kendra Collins, Stephen Hoy, Cassie Stark, Lake Graboski, Eric Jenkins, Thomas M. Saielli, Benjamin T. Jarrett, Lucinda J. Wigfield, Lauren M. Kerwien, Ciera Wilbur, Alexander M. Sandercock, J. Hill Craddock, Susanna Keriö, Tetyana Zhebentyayeva, Shenghua Fan, Austin M. Thomas, Albert G. Abbott, C. Dana Nelson, Xiaoxia Xia, James R. McKenna, Caleb Kell, Melissa Williams, LoriBeth Boston, Christopher Plott, Florian Carle, Jack Swatt, Jack Ostroff, Steven N. Jeffers, Kathleen McKeever, Erica Smith, Thomas J. Ellis, Joseph B. James, Paul Sisco, Andrew Newhouse, Erik Carlson, William A. Powell, Frederick V. Hebard, John Scrivani, Caragh Heverly, Martin Cipollini, Brian Clark, Eric Evans, Bruce Levine, John E. Carlson, David Goodstein, Jack Orebaugh, Zamin K. Yang, Madhavi Z. Martin, Joanna Tannous, Tomás A. Rush, Nancy L. Engle, Timothy J. Tschaplinski, Jane Grimwood, Jeremy Schmutz, Jason A. Holliday, John T. Lovell
More than a century after two introduced pathogens killed billions of American chestnut trees, introgression of resistance alleles from Chinese chestnuts has contributed to the recovery of self-sustaining populations. However, progress has been slow because of the complex genetic architecture of resistance. To better understand blight resistance, we compared reference genomes, gene expression responses, and stem metabolite profiles of the resistant Chinese and susceptible American chestnut species. To accelerate resistance breeding, we conducted large-scale phenotyping and genotyping in hybrids of these species. Simulation and inoculation experiments suggest that significant resistance gains are possible through selectively breeding trees with an average of 70 to 85% American chestnut ancestry. The resources developed in this work are foundational for breeding to create diverse restoration populations with sufficient disease resistance and competitive growth.
{"title":"Genomic approaches to accelerate American chestnut restoration","authors":"Jared W. Westbrook, Joanna Malukiewicz, Qian Zhang, Avinash Sreedasyam, Jerry W. Jenkins, Vasiliy Lakoba, Sara Fitzsimmons, Jamie Van Clief, Kendra Collins, Stephen Hoy, Cassie Stark, Lake Graboski, Eric Jenkins, Thomas M. Saielli, Benjamin T. Jarrett, Lucinda J. Wigfield, Lauren M. Kerwien, Ciera Wilbur, Alexander M. Sandercock, J. Hill Craddock, Susanna Keriö, Tetyana Zhebentyayeva, Shenghua Fan, Austin M. Thomas, Albert G. Abbott, C. Dana Nelson, Xiaoxia Xia, James R. McKenna, Caleb Kell, Melissa Williams, LoriBeth Boston, Christopher Plott, Florian Carle, Jack Swatt, Jack Ostroff, Steven N. Jeffers, Kathleen McKeever, Erica Smith, Thomas J. Ellis, Joseph B. James, Paul Sisco, Andrew Newhouse, Erik Carlson, William A. Powell, Frederick V. Hebard, John Scrivani, Caragh Heverly, Martin Cipollini, Brian Clark, Eric Evans, Bruce Levine, John E. Carlson, David Goodstein, Jack Orebaugh, Zamin K. Yang, Madhavi Z. Martin, Joanna Tannous, Tomás A. Rush, Nancy L. Engle, Timothy J. Tschaplinski, Jane Grimwood, Jeremy Schmutz, Jason A. Holliday, John T. Lovell","doi":"10.1126/science.adw3225","DOIUrl":"10.1126/science.adw3225","url":null,"abstract":"<div >More than a century after two introduced pathogens killed billions of American chestnut trees, introgression of resistance alleles from Chinese chestnuts has contributed to the recovery of self-sustaining populations. However, progress has been slow because of the complex genetic architecture of resistance. To better understand blight resistance, we compared reference genomes, gene expression responses, and stem metabolite profiles of the resistant Chinese and susceptible American chestnut species. To accelerate resistance breeding, we conducted large-scale phenotyping and genotyping in hybrids of these species. Simulation and inoculation experiments suggest that significant resistance gains are possible through selectively breeding trees with an average of 70 to 85% American chestnut ancestry. The resources developed in this work are foundational for breeding to create diverse restoration populations with sufficient disease resistance and competitive growth.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Edoardo Gianni, Samantha L Y Kwok, Christopher J K Wan, Kevin Goeij, Bryce E Clifton, Enrico S Colizzi, James Attwater, Philipp Holliger
The emergence of a chemical system capable of self-replication and evolution is a critical event in the origin of life. RNA polymerase ribozymes can replicate RNA, but their large size and structural complexity impede self-replication and preclude their spontaneous emergence. Here we describe QT45: a 45-nucleotide polymerase ribozyme, discovered from random sequence pools, that catalyzes general RNA-templated RNA synthesis using trinucleotide triphosphate (triplet) substrates in mildly alkaline eutectic ice. QT45 can synthesize both its complementary strand using a random triplet pool at 94.1% per-nucleotide fidelity, and a copy of itself using defined substrates, both with yields of ~0.2% in 72 days. The discovery of polymerase activity in a small RNA motif suggests that polymerase ribozymes are more abundant in RNA sequence space than previously thought.
{"title":"A small polymerase ribozyme that can synthesize itself and its complementary strand.","authors":"Edoardo Gianni, Samantha L Y Kwok, Christopher J K Wan, Kevin Goeij, Bryce E Clifton, Enrico S Colizzi, James Attwater, Philipp Holliger","doi":"10.1126/science.adt2760","DOIUrl":"https://doi.org/10.1126/science.adt2760","url":null,"abstract":"<p><p>The emergence of a chemical system capable of self-replication and evolution is a critical event in the origin of life. RNA polymerase ribozymes can replicate RNA, but their large size and structural complexity impede self-replication and preclude their spontaneous emergence. Here we describe QT45: a 45-nucleotide polymerase ribozyme, discovered from random sequence pools, that catalyzes general RNA-templated RNA synthesis using trinucleotide triphosphate (triplet) substrates in mildly alkaline eutectic ice. QT45 can synthesize both its complementary strand using a random triplet pool at 94.1% per-nucleotide fidelity, and a copy of itself using defined substrates, both with yields of ~0.2% in 72 days. The discovery of polymerase activity in a small RNA motif suggests that polymerase ribozymes are more abundant in RNA sequence space than previously thought.</p>","PeriodicalId":21678,"journal":{"name":"Science","volume":" ","pages":"eadt2760"},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146182107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dredging and mining river sediments can raise flood risks and threaten infrastructure, scientists say.
科学家说，疏浚和开采河流沉积物会增加洪水风险，并威胁到基础设施。
{"title":"Projects on silty Himalayan rivers raise alarms.","authors":"Athar Parvaiz","doi":"10.1126/science.aeg3558","DOIUrl":"https://doi.org/10.1126/science.aeg3558","url":null,"abstract":"<p><p>Dredging and mining river sediments can raise flood risks and threaten infrastructure, scientists say.</p>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":"644-645"},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146182050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L-Carnitine (the form of carnitine found in animals) transports long-chain fatty acids into mitochondria, where they go through β-oxidation, producing energy (1). This process occurs primarily in organs that use fat as energy, such as cardiac and skeletal muscles. For humans who eat meat, most carnitine is obtained from food. However, ~25% of the supply of carnitine in omnivorous humans relies on de novo synthesis, which reaches >90% among strict vegetarians or vegans. Endogenous carnitine is synthesized in the liver and kidneys from two methylated amino acids, lysine and methionine (1). This requires the transfer of trimethyllysine from the cytosol to the mitochondrial matrix (the innermost part of the mitochondria), for conversion into hydroxytrimethyllysine (2). On page 688 of this issue, Auger et al. (3) report that a mitochondrial trimethyllysine transporter, SLC25A45, has a key role in fat consumption in mice.
{"title":"The bottleneck of fat burning","authors":"Angela M. Ramos-Lobo, Pierre Maechler","doi":"10.1126/science.aef2173","DOIUrl":"10.1126/science.aef2173","url":null,"abstract":"<div >L-Carnitine (the form of carnitine found in animals) transports long-chain fatty acids into mitochondria, where they go through β-oxidation, producing energy (<i>1</i>). This process occurs primarily in organs that use fat as energy, such as cardiac and skeletal muscles. For humans who eat meat, most carnitine is obtained from food. However, ~25% of the supply of carnitine in omnivorous humans relies on de novo synthesis, which reaches >90% among strict vegetarians or vegans. Endogenous carnitine is synthesized in the liver and kidneys from two methylated amino acids, lysine and methionine (<i>1</i>). This requires the transfer of trimethyllysine from the cytosol to the mitochondrial matrix (the innermost part of the mitochondria), for conversion into hydroxytrimethyllysine (<i>2</i>). On page 688 of this issue, Auger <i>et al.</i> (<i>3</i>) report that a mitochondrial trimethyllysine transporter, SLC25A45, has a key role in fat consumption in mice.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Organisms have developed a variety of mechanisms to cope with potentially harmful mutations. These mechanisms include gene duplication, redundancy of metabolic factors or pathways, and feedback loops, all of which create backup systems and hidden reserves that ensure cellular stability (1). On page 687 of this issue, El-Brolosy et al. (2) report on transcriptional adaptation, a dual feedback and feedforward mechanism that uses genetic redundancy to compensate for mutations in protein-coding genes. The authors report that cells transport decay fragments of mutant messenger RNAs (mRNAs) from the cytoplasm to the nucleus to up-regulate the transcription of so-called “adapting genes”—the mutated gene; its paralogs (genes that originated from the same duplication event); and, in some cases, biologically related genes. El-Brolosy et al. also leveraged their mechanistic understanding of transcriptional regulation to develop short nucleic acid sequences that can artificially activate target gene expression in cells.
{"title":"Keeping cells fit","authors":"Xavier Rambout, Lynne E. Maquat","doi":"10.1126/science.aee7910","DOIUrl":"10.1126/science.aee7910","url":null,"abstract":"<div >Organisms have developed a variety of mechanisms to cope with potentially harmful mutations. These mechanisms include gene duplication, redundancy of metabolic factors or pathways, and feedback loops, all of which create backup systems and hidden reserves that ensure cellular stability (<i>1</i>). On page 687 of this issue, El-Brolosy <i>et al</i>. (<i>2</i>) report on transcriptional adaptation, a dual feedback and feedforward mechanism that uses genetic redundancy to compensate for mutations in protein-coding genes. The authors report that cells transport decay fragments of mutant messenger RNAs (mRNAs) from the cytoplasm to the nucleus to up-regulate the transcription of so-called “adapting genes”—the mutated gene; its paralogs (genes that originated from the same duplication event); and, in some cases, biologically related genes. El-Brolosy <i>et al</i>. also leveraged their mechanistic understanding of transcriptional regulation to develop short nucleic acid sequences that can artificially activate target gene expression in cells.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RNA comes close to copying itself","authors":"Robert F. Service","doi":"10.1126/science.aeg3559","DOIUrl":"10.1126/science.aeg3559","url":null,"abstract":"","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Donia Arafa, Julia van de Korput, Philipp N. Braaker, Kieran P. Higgins, Niels R. C. Meijns, Katy L. H. Marshall-Phelps, Julia Meng, Daniel Soong, Eleonora Scalia, Kyle Lathem, Marcus Keatinge, Claire Richmond, Anna Klingseisen, Marja Main, Sarah A. Neely, David W. Hampton, Greg J. Duncan, Geert J. Schenk, Marie Louise Groot, Siddharthan Chandran, Ben Emery, Antonio Luchicchi, Maarten H. P. Kole, Anna C. Williams, David A. Lyons
Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood. In this study, we found that early damage in zebrafish and rodent demyelination models is characterized by myelin swelling. We show, through live imaging, that myelin swelling does not always lead to myelin loss and that swellings can sometimes resolve, allowing sheaths to remodel. Increased neuronal activity during early demyelination exacerbates myelin damage, whereas reducing neuronal activity mitigates myelin swelling in both zebrafish and mice. In human multiple sclerosis tissue, myelin swelling is also dynamic and is prominent around active lesions. Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.
{"title":"Myelin sheaths in the central nervous system can withstand damage and dynamically remodel","authors":"Donia Arafa, Julia van de Korput, Philipp N. Braaker, Kieran P. Higgins, Niels R. C. Meijns, Katy L. H. Marshall-Phelps, Julia Meng, Daniel Soong, Eleonora Scalia, Kyle Lathem, Marcus Keatinge, Claire Richmond, Anna Klingseisen, Marja Main, Sarah A. Neely, David W. Hampton, Greg J. Duncan, Geert J. Schenk, Marie Louise Groot, Siddharthan Chandran, Ben Emery, Antonio Luchicchi, Maarten H. P. Kole, Anna C. Williams, David A. Lyons","doi":"10.1126/science.adr4661","DOIUrl":"10.1126/science.adr4661","url":null,"abstract":"<div >Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood. In this study, we found that early damage in zebrafish and rodent demyelination models is characterized by myelin swelling. We show, through live imaging, that myelin swelling does not always lead to myelin loss and that swellings can sometimes resolve, allowing sheaths to remodel. Increased neuronal activity during early demyelination exacerbates myelin damage, whereas reducing neuronal activity mitigates myelin swelling in both zebrafish and mice. In human multiple sclerosis tissue, myelin swelling is also dynamic and is prominent around active lesions. Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号