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Clusterin induced by OPC phagocytosis blocks IL-9 secretion to inhibit myelination in a model of Alzheimer's disease

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Heliyon 2025年第1期11卷 e41635页

作者： Beiter, Rebecca M. Raghavan, Tula P. Suchocki, Olivia Ennerfelt, Hannah E. Rivet-Noor, Courtney R. Merchak, Andrea R. Phillips, Jennifer L. Bathe, Tim Lukens, John R. Prokop, Stefan Dupree, Jeffrey L. Gaultier, Alban Center for Brain Immunology and Glia Department of Neuroscience Charlottesville 22908 VA United States Graduate Program in Neuroscience Charlottesville 22908 VA United States Department of Neurobiology UMass Chan Medical School Worcester 01655 MA United States Medical Scientist Training Program University of Virginia School of Medicine Charlottesville 22908 VA United States Center for Translational Research in Neurodegenerative Disease College of Medicine University of Florida Gainesville 32610 FL United States Department of Pathology College of Medicine University of Florida Gainesville 32610 United States McKnight Brain Institute College of Medicine University of Florida Gainesville 32610 FL United States Department of Anatomy and Neurobiology Virginia Commonwealth University Richmond 23298 VA United States

Background: Variants in the CLUSTERIN gene have been identified as a risk factor for late-onset Alzheimer's disease and are linked to decreased white matter integrity in healthy adults. However, the specific role for clusterin in myelin maintenance in the context of Alzheimer's disease remains unclear. Methods: We employed a combination of immunofluorescence and transmission electron microscopy techniques, primary culture of OPCs, and an animal model of Alzheimer's disease. Results: We found that phagocytosis of debris such as amyloid beta, myelin, and apoptotic cells, increases clusterin expression in oligodendrocyte progenitors. We further discovered that exposure to clusterin inhibits differentiation of oligodendrocyte progenitors. Mechanistically, clusterin blunts production of IL-9 and addition of exogenous IL-9 can rescue clusterin-inhibited myelination. Lastly, we demonstrate that clusterin deletion in mice prevents myelin loss in the 5XFAD model. Discussion: Our data suggest that clusterin could play a key role in Alzheimer's disease myelin pathology. © 2025 The Authors

关键词： Alzheimer's disease Astrocyte Clusterin IL-9 Myelin Oligodendrocyte progenitor cells

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Polyvalvular Dysplasia and Vascular Abnormalities in a Neonate With an FLNA Variant

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JACC: Case Reports 2024年第18期29卷 102556-102556页

作者： Frenkel, Amy Frenkel, Max Schulte, Jefree J. Srinivasan, Shardha Lamers, Luke School of Medicine and Public Health University of Wisconsin Madison WI United States Cellular and Molecular Biology Graduate Program University of Wisconsin Madison WI United States Medical Scientist Training Program University of Wisconsin Madison WI United States Department of Pathology and Laboratory Medicine School of Medicine and Public Health University of Wisconsin Madison WI United States Division of Cardiology Department of Pediatrics School of Medicine and Public Health University of Wisconsin Madison WI United States

There is growing appreciation for inherited structural heart diseases and their genetic causes. One causal gene for congenital cardiac and vascular lesions is FLNA which encodes a critical protein for cytoskeletal and extracellular matrix development. A newborn infant male, with prenatally diagnosed polyvalvular dysfunction, presented with low cardiac output and postnatally detected aortic arch hypoplasia and coarctation. Attempted palliative coarctation intervention resulted in vascular complications that ultimately contributed to his demise. This case report highlights polyvalvular dysplasia, vascular abnormalities, and a likely causal de novo missense variant in the FLNA gene (c.5180 C>T p.P1727L) not previously described. © 2024 The Authors

关键词： cardiac catheterization filamin A variant effect prediction vasculopathy

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Microwell-Patterned Microfluidic Device for Rapid Identification of High-Affinity Anti-Tumor T Cells

Microwell-Patterned Microfluidic Device for Rapid Identifica...

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IEEE International Conference on Micro Electro Mechanical Systems

作者： Kavya L. Singampalli Desh Deepak Dixit Peixin Jiang Alexandre Reuben Peter B. Lillehoj Department of Bioengineering Rice University Houston TX USA Medical Scientist Training Program Baylor College of Medicine Houston TX USA Department of Mechanical Engineering Rice University Houston TX USA Department of Thoracic/ Head and Neck Medical Oncology The University of Texas MD Anderson Cancer Center Houston TX USA The University of Texas MD Anderson Cancer Center UT Health Houston Graduate School of Biomedical Sciences Houston TX USA

This paper presents a microfluidic device for the rapid identification of high-affinity anti-tumor T cells. This device consists of a polymethyl methacrylate (PMMA) microchannel containing a dense array of circular microwells fabricated using a unique CO 2 laser etching process. Using this device, OT-I T cells and LLC-OVA tumor cells were incubated within microwells to identify high-affinity T cells in <1 hour, which is significantly faster than existing T cell screening methods (requiring weeks/months) while being simpler to operate without requiring sophisticated instrumentation. Furthermore, this method is compatible with adherent and nonadherent tumor cells, making it a versatile platform for T cell-tumor cell interaction studies and T cell screening.

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Computational design of serine hydrolases

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Science (New York, N.Y.) 2025年第6744期388卷 eadu2454页

作者： Lauko, Anna Pellock, Samuel J. Sumida, Kiera H. Anishchenko, Ivan Juergens, David Ahern, Woody Jeung, Jihun Shida, Alexander F. Hunt, Andrew Kalvet, Indrek Norn, Christoffer Humphreys, Ian R. Jamieson, Cooper Krishna, Rohith Kipnis, Yakov Kang, Alex Brackenbrough, Evans Bera, Asim K. Sankaran, Banumathi Houk, K.N. Baker, David Department of Biochemistry University of Washington Seattle WA United States Institute for Protein Design University of Washington Seattle WA United States Graduate Program in Biological Physics Structure and Design University of Washington Seattle WA United States Department of Chemistry University of Washington Seattle WA United States Graduate Program in Molecular Engineering University of Washington Seattle WA United States Paul G. Allen School of Computer Science and Engineering University of Washington Seattle WA United States Medical Scientist Training Program University of Washington Seattle WA United States Howard Hughes Medical Institute University of Washington Seattle WA United States Department of Chemistry and Biochemistry University of California Los Angeles CA United States

The design of enzymes with complex active sites that mediate multistep reactions remains an outstanding challenge. With serine hydrolases as a model system, we combined the generative capabilities of RFdiffusion with an ensemble generation method for assessing active site preorganization at each step in the reaction to design enzymes starting from minimal active site descriptions. Experimental characterization revealed catalytic efficiencies (kcat/Km) up to 2.2 × 105 M-1 s-1 and crystal structures that closely match the design models (Cα root mean square deviations <1 angstrom). Selection for structural compatibility across the reaction coordinate enabled identification of new catalysts remove with five different folds distinct from those of natural serine hydrolases. Our de novo approach provides insight into the geometric basis of catalysis and a roadmap for designing enzymes that catalyze multistep transformations.

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BPS2025 - Disaggregation of biomolecular condensates by molecular chaperones is heterogeneous at the single-condensate level

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Biophysical Journal 2025年第3期124卷 415a-415a页

作者： Diangen Lin Kyle M. Lin David A. Drummond Allison H. Squires Harvard Graduate Program in Biophysics Harvard University Cambridge MA USA Graduate Program in Biophysical Sciences Medical Scientist Training Program University of Chicago Chicago IL USA Department of Biochemistry and Molecular Biology and Department of Medicine Section of Genetic Medicine University of Chicago Chicago IL USA Pritzker School of Molecular Engineering University of Chicago Chicago IL USA

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Correction to: Multistate and functional protein design using RoseTTAFold sequence space diffusion (Nature Biotechnology, (2024), 10.1038/s41587-024-02395-w)

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Nature Biotechnology 2024年

作者： Lisanza, Sidney Lyayuga Gershon, Jacob Merle Tipps, Samuel W. K. Sims, Jeremiah Nelson Arnoldt, Lucas Hendel, Samuel J. Simma, Miriam K. Liu, Ge Yase, Muna Wu, Hongwei Tharp, Claire D. Li, Xinting Kang, Alex Brackenbrough, Evans Bera, Asim K. Gerben, Stacey Wittmann, Bruce J. McShan, Andrew C. Baker, David Department of Biochemistry University of Washington SeattleWA United States Institute for Protein Design University of Washington SeattleWA United States Graduate Program in Biological Physics Structure and Design University of Washington SeattleWA United States Department of Molecular Engineering University of Washington SeattleWA United States Molecular & amp Cellular Biology Medical Scientist Training Program University of Washington SeattleWA United States Faculty of Engineering Sciences Heidelberg University Heidelberg Germany School of Chemistry and Biochemistry Georgia Institute of Technology AtlantaGA United States Office of the Chief Scientific Officer Microsoft RedmondWA United States Howard Hughes Medical Institute University of Washington SeattleWA United States

Correction to: Nature Biotechnologyhttps://***/10.1038/s41587-024-02395-w, published online 25 September 2024. In the version of the article initially published, in the key to Fig. 2f the colors were swapped and have now been amended so that "W guidance" is purple and "Unconditional" is grey. In Fig. 5a, the color of "Child B" has been corrected from pink to purple, and in Fig. 5d, "β-helix" has now been amended to "β-sheet". These corrections have been made to the HTML and PDF versions of the article. © The Author(s) 2024.

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RHOA deficiency drives decreased CD19 expression and immune dysregulation in CAR-T resistant diffuse large B-cell lymphoma

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Hematological Oncology 2023年第S2期41卷

作者： A. Newsam C. Coughlin Y. Goretsky A. Sondhi E. Roberts D. Bilbao B. Ziccheddu P. Manera F. Maura J. Schatz University of Miami Miller School of Medicine Medical Scientist Training Program Miami USA University of Miami Miller School of Medicine Medicine Miami USA University of Miami Miller School of Medicine Cancer Biology Graduate Program Miami USA

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Integrated information theory (IIT) 4.0: Formulating the properties of phenomenal existence in physical terms

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PLoS Computational Biology 2023年第10 October期19卷 e1011465-e1011465页

作者： Albantakis, Larissa Barbosa, Leonardo Findlay, Graham Grasso, Matteo Haun, Andrew M. Marshall, William Mayner, William G.P. Zaeemzadeh, Alireza Boly, Melanie Juel, Bjørn E. Sasai, Shuntaro Fujii, Keiko David, Isaac Hendren, Jeremiah Lang, Jonathan P. Tononi, Giulio Department of Psychiatry University of Wisconsin MadisonWI United States Fralin Biomedical Research Institute at VTC Virginia Tech RoanokeVA United States Neuroscience Training Program University of Wisconsin MadisonWI United States Department of Mathematics and Statistics Brock University St. CatharinesON Canada Department of Neurology University of Wisconsin MadisonWI United States Institute of Basic Medical Sciences University of Oslo Oslo Norway Araya Inc Tokyo Japan Graduate School Language & Literature Ludwig Maximilian University of Munich Munich Germany

This paper presents Integrated Information Theory (IIT) 4.0. IIT aims to account for the properties of experience in physical (operational) terms. It identifies the essential properties of experience (axioms), infers the necessary and sufficient properties that its substrate must satisfy (postulates), and expresses them in mathematical terms. In principle, the postulates can be applied to any system of units in a state to determine whether it is conscious, to what degree, and in what way. IIT offers a parsimonious explanation of empirical evidence, makes testable predictions concerning both the presence and the quality of experience, and permits inferences and extrapolations. IIT 4.0 incorporates several developments of the past ten years, including a more accurate formulation of the axioms as postulates and mathematical expressions, the introduction of a unique measure of intrinsic information that is consistent with the postulates, and an explicit assessment of causal relations. By fully unfolding a system’s irreducible cause–effect power, the distinctions and relations specified by a substrate can account for the quality of experience. Copyright: © 2023 Albantakis et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

关键词： Information theory

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Correction: SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex

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Acta neuropathologica communications 2024年第1期12卷 92页

作者： Jennifer L Brown Damyan W Hart Gabriel E Boyle Taylor G Brown Michael LaCroix Andrés M Baraibar Ross Pelzel Minwoo Kim Mathew A Sherman Samuel Boes Michelle Sung Tracy Cole Michael K Lee Alfonso Araque Sylvain E Lesné Graduate Program in Neuroscience University of Minnesota Minneapolis MN USA. Department of Neuroscience University of Minnesota Minneapolis MN USA. Institute for Translational Neuroscience University of Minnesota Wallin Medical Biosciences Building (Room 4-114) 2101 Sixth Street SE CDC 2641 Minneapolis MN 55414 USA. Graduate Program in Molecular and Cellular Biology University of Washington Seattle WA 98195 USA. Medical Scientist Training Program University of Minnesota Minneapolis MN USA. Medical Scientist Training Program University of Texas Southwestern Medical School Dallas TX 75390 USA. Department of Neurosciences University of the Basque Country UPV/EHU Leioa Spain. Bloomberg School of Public Health Johns Hopkins University Baltimore MD 21218 USA. Ionis Pharmaceuticals Inc. Carlsbad CA USA. n-Lorem Foundation Carlsbad CA 92010 USA. Graduate Program in Neuroscience University of Minnesota Minneapolis MN USA. lesne002@umn.edu. Department of Neuroscience University of Minnesota Minneapolis MN USA. lesne002@umn.edu. Institute for Translational Neuroscience University of Minnesota Wallin Medical Biosciences Building (Room 4-114) 2101 Sixth Street SE CDC 2641 Minneapolis MN 55414 USA. lesne002@umn.edu.

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Systemic factors as mediators of brain homeostasis, ageing and neurodegeneration (vol 21, pg 93, 2020)

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NATURE REVIEWS neuroscience 2020年第5期21卷 298-298页

作者： Pluvinage, John V. Wyss-Coray, Tony Medical Scientist Training Program Stanford University School of Medicine Stanford CA USA Stem Cell Biology and Regenerative Medicine Graduate Program Stanford University School of Medicine Stanford CA USA Department of Neurology and Neurological Sciences Stanford University School of Medicine Stanford CA USA Veterans Administration Palo Alto Healthcare System Palo Alto CA USA Paul F. Glenn Center for the Biology of Aging Stanford University School of Medicine Stanford CA USA Wu Tsai Neurosciences Institute Stanford University Stanford CA USA

A rapidly ageing population and a limited therapeutic toolbox urgently necessitate new approaches to treat neurodegenerative diseases. Brain ageing, the key risk factor for neurodegeneration, involves complex cellular and molecular processes that eventually result in cognitive decline. Although cell-intrinsic defects in neurons and glia may partially explain this decline, cell-extrinsic changes in the systemic environment, mediated by blood, have recently been shown to contribute to brain dysfunction with age. Here, we review the current understanding of how systemic factors mediate brain ageing, how these factors are regulated and how we can translate these findings into therapies for neurodegenerative diseases.

关键词： Alzheimer's disease Neural ageing Neuroimmunology Parkinson's disease

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