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Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Aβ1-42 and mutant Tau.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Aβ1-42 and mutant Tau.
Συγγραφείς: Hirsch F; Department of Cell Biology, University of Bremen, Leobener Strasse 2, 28359 Bremen, Germany., F Läubli N; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK., Kelkar A; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Sleiman M; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Woitzat Y; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Gallrein C; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Gumz V; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Kalsi GK; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany., Fernandez-Villegas A; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK., Schierle GSK; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK., Kirstein J; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.; Friedrich-Schiller-Universität, Institute for Biochemistry & Biophysics, Hans Knöll-Strasse 2, 07745 Jena, Germany.
Πηγή: Disease models & mechanisms [Dis Model Mech] 2026 Mar 01; Vol. 19 (3). Date of Electronic Publication: 2026 Apr 01.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Company of Biologists Ltd Country of Publication: England NLM ID: 101483332 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1754-8411 (Electronic) Linking ISSN: 17548403 NLM ISO Abbreviation: Dis Model Mech Subsets: MEDLINE
Imprint Name(s): Original Publication: Cambridge : Company of Biologists Ltd., c2008-
Ιατρικοί όροι (MeSH): Amyloid beta-Peptides*/metabolism , tau Proteins*/metabolism , tau Proteins*/genetics , Neurons*/metabolism , Neurons*/pathology , Mutation*/genetics , Peptide Fragments*/metabolism , Mutant Proteins*/metabolism , Protein Aggregates* , Protein Aggregation, Pathological*, Caenorhabditis elegans/metabolism ; Aging/pathology ; Aging/metabolism ; Muscles/metabolism ; Muscles/pathology ; Calcium/metabolism ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Proteotoxic Stress
Περίληψη: Alzheimer's disease (AD) is a progressive neurodegenerative disease that is characterized by the accumulation of amyloid-β (Aβ) plaques and neurofibrillary Tau tangles, ultimately leading to brain atrophy and death. To elucidate the relationship between the aberrant folding and aggregation of Aβ and mutant Tau and neuronal function, we monitored neuronal activity in C. elegans AD models across age. For that, we used a neuronal GCaMP reporter to monitor fluctuations in Ca2+ and developed microfluidic devices to immobilize nematodes to non-invasively assess neuronal activity. Our findings revealed that expression of both Aβ and Tau lead to significant reductions in neuronal activity and function in young adult animals, preceding the accumulation of amyloid aggregates. Notably, Aβ expression and aggregation in muscle tissue produced detrimental effects on neuronal activity comparable to those seen after expression in neurons, suggesting that proteotoxic stress in muscle can influence neuronal function. This may occur through propagation of Aβ from muscle to neurons or through retrograde signaling pathways. Further, our new sub-stoichiometrically labeled Tau strains highlight the significant impact TauP301L,V337M has on neuronal activity throughout aging. These results enhance our understanding of the early functional effects of amyloid aggregation in Alzheimer's disease.
(© 2026. Published by The Company of Biologists.)
Competing Interests: Competing interests The authors declare no competing or financial interests.
Σχόλια: Update of: bioRxiv. 2025 Jul 24:2025.07.21.665894. doi: 10.1101/2025.07.21.665894.. (PMID: 40777286)
References: Gene. 1999 Mar 18;229(1-2):31-5. (PMID: 10095101)
Front Aging Neurosci. 2022 Jul 06;14:946297. (PMID: 35928998)
Nano Lett. 2017 Jan 11;17(1):143-149. (PMID: 28073262)
Nature. 2006 May 4;441(7089):91-5. (PMID: 16672971)
Science. 2017 Jun 23;356(6344):. (PMID: 28642382)
J Cell Sci. 2013 May 1;126(Pt 9):2079-91. (PMID: 23525010)
Prog Neurobiol. 2021 Mar;198:101907. (PMID: 32926945)
PLoS One. 2013 May 22;8(5):e64297. (PMID: 23717588)
Front Aging. 2022 Aug 19;3:928574. (PMID: 36062211)
Am J Pathol. 2000 Jul;157(1):277-86. (PMID: 10880397)
J Cell Sci. 1996 Nov;109 ( Pt 11):2661-72. (PMID: 8937984)
Cell. 2010 Nov 24;143(5):813-25. (PMID: 21111239)
Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9980-5. (PMID: 12872001)
Transl Psychiatry. 2022 Jun 22;12(1):257. (PMID: 35732622)
Dev Cell. 2017 Jan 23;40(2):202-214. (PMID: 28041904)
PLoS One. 2014 Dec 03;9(12):e113917. (PMID: 25470130)
Front Physiol. 2023 Jul 04;14:1228490. (PMID: 37469564)
Nat Commun. 2021 May 10;12(1):2583. (PMID: 33972516)
J Biol Methods. 2014;1(2):. (PMID: 25606571)
Hum Mol Genet. 2012 Aug 15;21(16):3587-603. (PMID: 22611162)
Neurobiol Dis. 2005 Nov;20(2):372-83. (PMID: 16242642)
Nat Commun. 2016 Oct 11;7:13023. (PMID: 27725672)
J Biol Chem. 2009 Mar 6;284(10):6021-5. (PMID: 18948254)
Nature. 2013 Jul 18;499(7458):295-300. (PMID: 23868258)
Nat Rev Mol Cell Biol. 2014 Mar;15(3):211-7. (PMID: 24556842)
Lab Chip. 2007 Nov;7(11):1515-23. (PMID: 17960280)
CNS Neurosci Ther. 2011 Oct;17(5):514-24. (PMID: 20553310)
Oncotarget. 2016 Aug 30;7(35):56147-56152. (PMID: 27528229)
Lab Chip. 2010 Jul 21;10(14):1862-8. (PMID: 20461264)
Biochemistry. 2004 Feb 17;43(6):1694-703. (PMID: 14769047)
Neurobiol Dis. 2018 Sep;117:226-234. (PMID: 29936232)
Development. 2003 Aug;130(16):3781-94. (PMID: 12835394)
Lab Chip. 2009 Jan 7;9(1):151-7. (PMID: 19209348)
Mol Neurodegener. 2016 Apr 27;11:33. (PMID: 27118310)
WormBook. 2013 Sep 24;:1-19. (PMID: 24065448)
Cell. 2013 Jun 6;153(6):1366-78. (PMID: 23746847)
Front Mol Neurosci. 2021 Oct 15;14:721749. (PMID: 34720872)
Ann Med. 1989;21(2):127-32. (PMID: 2504257)
Molecules. 2019 Nov 25;24(23):. (PMID: 31775328)
PLoS One. 2013 Oct 09;8(10):e76019. (PMID: 24130756)
Lab Chip. 2012 Jun 21;12(12):2211-20. (PMID: 22588281)
Neuron. 2007 Feb 1;53(3):337-51. (PMID: 17270732)
Neuron. 2017 Feb 8;93(3):533-541.e5. (PMID: 28111080)
Proc Natl Acad Sci U S A. 2007 Aug 28;104(35):13891-5. (PMID: 17715055)
Neurology. 2005 Aug 9;65(3):404-11. (PMID: 16087905)
Nat Neurosci. 1999 Nov;2(11):959-64. (PMID: 10526333)
N Engl J Med. 2000 Aug 17;343(7):450-6. (PMID: 10944562)
J Vis Exp. 2020 Mar 27;(157):. (PMID: 32281971)
Am J Pathol. 2007 Sep;171(3):976-92. (PMID: 17690183)
Cold Spring Harb Protoc. 2012 Jun 01;2012(6):647-56. (PMID: 22661439)
Grant Information: KI1988/7-1 Deutsche Forschungsgemeinschaft; MR/K02292X/1 United Kingdom MRF_ MRF_; ARUK-PG013-14 Alzheimer's Research UK; 20052CB Alzheimer Forschung Initiative; Universität Bremen; KI1988/7-1 Deutsche Forschungsgemeinschaft (DFG); 065807/Z/01/Z United Kingdom WT_ Wellcome Trust; 203249/Z/16/Z United Kingdom WT_ Wellcome Trust; MR/K02292X/1 Medical Research Council (MRC); ARUK-PG013-14 Alzheimer Research UK (ARUK); 16238 Michael J. Fox Foundation
Contributed Indexing: Keywords: C. elegans; Abeta; Aging; Alzheimers disease; Neurodegeneration; Tau
Substance Nomenclature: 0 (Amyloid beta-Peptides)
0 (tau Proteins)
0 (amyloid beta-protein (1-42))
0 (Peptide Fragments)
0 (Protein Aggregates)
0 (Mutant Proteins)
SY7Q814VUP (Calcium)
Entry Date(s): Date Created: 20260223 Date Completed: 20260708 Latest Revision: 20260813
Update Code: 20260813
PubMed Central ID: PMC13072132
DOI: 10.1242/dmm.052295
PMID: 41725344
Βάση Δεδομένων: MEDLINE
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  Label: Title
  Group: Ti
  Data: Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Aβ1-42 and mutant Tau.
– Name: Author
  Label: Authors
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  Data: <searchLink fieldCode="AU" term="%22Hirsch+F%22">Hirsch F</searchLink>; Department of Cell Biology, University of Bremen, Leobener Strasse 2, 28359 Bremen, Germany.<br /><searchLink fieldCode="AU" term="%22F+Läubli+N%22">F Läubli N</searchLink>; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK.<br /><searchLink fieldCode="AU" term="%22Kelkar+A%22">Kelkar A</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Sleiman+M%22">Sleiman M</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Woitzat+Y%22">Woitzat Y</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Gallrein+C%22">Gallrein C</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Gumz+V%22">Gumz V</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Kalsi+GK%22">Kalsi GK</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.<br /><searchLink fieldCode="AU" term="%22Fernandez-Villegas+A%22">Fernandez-Villegas A</searchLink>; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK.<br /><searchLink fieldCode="AU" term="%22Schierle+GSK%22">Schierle GSK</searchLink>; Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, Philippa-Fawcett Drive, Cambridge CB3 0AS, UK.<br /><searchLink fieldCode="AU" term="%22Kirstein+J%22">Kirstein J</searchLink>; Leibniz Institute on Aging - Fritz-Lipmann-Institute, Beutenbergstrasse 11, 07745 Jena, Germany.; Friedrich-Schiller-Universität, Institute for Biochemistry & Biophysics, Hans Knöll-Strasse 2, 07745 Jena, Germany.
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  Data: <searchLink fieldCode="JN" term="%22101483332%22">Disease models & mechanisms</searchLink> [Dis Model Mech] 2026 Mar 01; Vol. 19 (3). <i>Date of Electronic Publication: </i>2026 Apr 01.
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  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22Company+of+Biologists+Ltd%22">Company of Biologists Ltd </searchLink><i>Country of Publication: </i>England <i>NLM ID: </i>101483332 <i>Publication Model: </i>Print-Electronic <i>Cited Medium: </i>Internet <i>ISSN: </i>1754-8411 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2217548403%22">17548403 </searchLink><i>NLM ISO Abbreviation: </i>Dis Model Mech <i>Subsets: </i>MEDLINE
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  Data: <i>Original Publication</i>: Cambridge : Company of Biologists Ltd., c2008-
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  Data: <searchLink fieldCode="MM" term="%22Amyloid+beta-Peptides%22">Amyloid beta-Peptides*</searchLink>/<searchLink fieldCode="MM" term="%22Amyloid+beta-Peptides+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22tau+Proteins%22">tau Proteins*</searchLink>/<searchLink fieldCode="MM" term="%22tau+Proteins+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22tau+Proteins%22">tau Proteins*</searchLink>/<searchLink fieldCode="MM" term="%22tau+Proteins+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurons%22">Neurons*</searchLink>/<searchLink fieldCode="MM" term="%22Neurons+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurons%22">Neurons*</searchLink>/<searchLink fieldCode="MM" term="%22Neurons+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Mutation%22">Mutation*</searchLink>/<searchLink fieldCode="MM" term="%22Mutation+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Peptide+Fragments%22">Peptide Fragments*</searchLink>/<searchLink fieldCode="MM" term="%22Peptide+Fragments+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Mutant+Proteins%22">Mutant Proteins*</searchLink>/<searchLink fieldCode="MM" term="%22Mutant+Proteins+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Protein+Aggregates%22">Protein Aggregates*</searchLink> <br /><searchLink fieldCode="MM" term="%22Protein+Aggregation%2C+Pathological%22">Protein Aggregation, Pathological*</searchLink><br /><searchLink fieldCode="MH" term="%22Caenorhabditis+elegans%22">Caenorhabditis elegans</searchLink>/<searchLink fieldCode="MH" term="%22Caenorhabditis+elegans+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Aging%22">Aging</searchLink>/<searchLink fieldCode="MH" term="%22Aging+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Aging%22">Aging</searchLink>/<searchLink fieldCode="MH" term="%22Aging+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Muscles%22">Muscles</searchLink>/<searchLink fieldCode="MH" term="%22Muscles+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Muscles%22">Muscles</searchLink>/<searchLink fieldCode="MH" term="%22Muscles+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Calcium%22">Calcium</searchLink>/<searchLink fieldCode="MH" term="%22Calcium+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Alzheimer+Disease%22">Alzheimer Disease</searchLink>/<searchLink fieldCode="MH" term="%22Alzheimer+Disease+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Alzheimer+Disease%22">Alzheimer Disease</searchLink>/<searchLink fieldCode="MH" term="%22Alzheimer+Disease+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Proteotoxic+Stress%22">Proteotoxic Stress</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Alzheimer's disease (AD) is a progressive neurodegenerative disease that is characterized by the accumulation of amyloid-β (Aβ) plaques and neurofibrillary Tau tangles, ultimately leading to brain atrophy and death. To elucidate the relationship between the aberrant folding and aggregation of Aβ and mutant Tau and neuronal function, we monitored neuronal activity in C. elegans AD models across age. For that, we used a neuronal GCaMP reporter to monitor fluctuations in Ca2+ and developed microfluidic devices to immobilize nematodes to non-invasively assess neuronal activity. Our findings revealed that expression of both Aβ and Tau lead to significant reductions in neuronal activity and function in young adult animals, preceding the accumulation of amyloid aggregates. Notably, Aβ expression and aggregation in muscle tissue produced detrimental effects on neuronal activity comparable to those seen after expression in neurons, suggesting that proteotoxic stress in muscle can influence neuronal function. This may occur through propagation of Aβ from muscle to neurons or through retrograde signaling pathways. Further, our new sub-stoichiometrically labeled Tau strains highlight the significant impact TauP301L,V337M has on neuronal activity throughout aging. These results enhance our understanding of the early functional effects of amyloid aggregation in Alzheimer's disease.<br /> (© 2026. Published by The Company of Biologists.)
– Name: Abstract
  Label: Competing Interests
  Group: Ab
  Data: Competing interests The authors declare no competing or financial interests.
– Name: Comment
  Label: Comments
  Group: Commnt
  Data: Update of: bioRxiv. 2025 Jul 24:2025.07.21.665894. doi: 10.1101/2025.07.21.665894.. (PMID: <searchLink fieldCode="PM" term="%2240777286%22">40777286)</searchLink>
– Name: Ref
  Label: References
  Group: RefInfo
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(PMID: <searchLink fieldCode="PM" term="%2223717588%22">23717588)</searchLink><br />Front Aging. 2022 Aug 19;3:928574. (PMID: <searchLink fieldCode="PM" term="%2236062211%22">36062211)</searchLink><br />Am J Pathol. 2000 Jul;157(1):277-86. (PMID: <searchLink fieldCode="PM" term="%2210880397%22">10880397)</searchLink><br />J Cell Sci. 1996 Nov;109 ( Pt 11):2661-72. (PMID: <searchLink fieldCode="PM" term="%228937984%22">8937984)</searchLink><br />Cell. 2010 Nov 24;143(5):813-25. (PMID: <searchLink fieldCode="PM" term="%2221111239%22">21111239)</searchLink><br />Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9980-5. (PMID: <searchLink fieldCode="PM" term="%2212872001%22">12872001)</searchLink><br />Transl Psychiatry. 2022 Jun 22;12(1):257. (PMID: <searchLink fieldCode="PM" term="%2235732622%22">35732622)</searchLink><br />Dev Cell. 2017 Jan 23;40(2):202-214. (PMID: <searchLink fieldCode="PM" term="%2228041904%22">28041904)</searchLink><br />PLoS One. 2014 Dec 03;9(12):e113917. 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– Name: GrantInfo
  Label: Grant Information
  Group: Grant
  Data: KI1988/7-1 Deutsche Forschungsgemeinschaft; MR/K02292X/1 United Kingdom MRF_ MRF_; ARUK-PG013-14 Alzheimer's Research UK; 20052CB Alzheimer Forschung Initiative; Universität Bremen; KI1988/7-1 Deutsche Forschungsgemeinschaft (DFG); 065807/Z/01/Z United Kingdom WT_ Wellcome Trust; 203249/Z/16/Z United Kingdom WT_ Wellcome Trust; MR/K02292X/1 Medical Research Council (MRC); ARUK-PG013-14 Alzheimer Research UK (ARUK); 16238 Michael J. Fox Foundation
– Name: SubjectMinor
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  Group:
  Data: <i>Keywords: </i>C. elegans; Abeta; Aging; Alzheimers disease; Neurodegeneration; Tau
– Name: NumberCAS
  Label: Substance Nomenclature
  Group: ID
  Data: 0 (Amyloid beta-Peptides)<br />0 (tau Proteins)<br />0 (amyloid beta-protein (1-42))<br />0 (Peptide Fragments)<br />0 (Protein Aggregates)<br />0 (Mutant Proteins)<br />SY7Q814VUP (Calcium)
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  Data: <i>Date Created: </i>20260223 <i>Date Completed: </i>20260708 <i>Latest Revision: </i>20260813
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  Group: Date
  Data: 20260813
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  Data: PMC13072132
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  Data: 10.1242/dmm.052295
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  Data: 41725344
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=cmedm&AN=41725344
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      – Type: doi
        Value: 10.1242/dmm.052295
    Languages:
      – Code: eng
        Text: English
    Subjects:
      – SubjectFull: Caenorhabditis elegans metabolism
        Type: general
      – SubjectFull: Aging pathology
        Type: general
      – SubjectFull: Aging metabolism
        Type: general
      – SubjectFull: Muscles metabolism
        Type: general
      – SubjectFull: Muscles pathology
        Type: general
      – SubjectFull: Calcium metabolism
        Type: general
      – SubjectFull: Alzheimer Disease metabolism
        Type: general
      – SubjectFull: Alzheimer Disease pathology
        Type: general
      – SubjectFull: Animals
        Type: general
      – SubjectFull: Proteotoxic Stress
        Type: general
      – SubjectFull: Amyloid beta-Peptides metabolism
        Type: general
      – SubjectFull: tau Proteins metabolism
        Type: general
      – SubjectFull: tau Proteins genetics
        Type: general
      – SubjectFull: Neurons metabolism
        Type: general
      – SubjectFull: Neurons pathology
        Type: general
      – SubjectFull: Mutation genetics
        Type: general
      – SubjectFull: Peptide Fragments metabolism
        Type: general
      – SubjectFull: Mutant Proteins metabolism
        Type: general
      – SubjectFull: Protein Aggregates
        Type: general
      – SubjectFull: Protein Aggregation, Pathological
        Type: general
    Titles:
      – TitleFull: Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Aβ1-42 and mutant Tau.
        Type: main
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            – D: 01
              M: 03
              Text: 2026 Mar 01
              Type: published
              Y: 2026
          Identifiers:
            – Type: issn-electronic
              Value: 1754-8411
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              Value: 19
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            – TitleFull: Disease models & mechanisms
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