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  1. Book: Inclusion body myositis

    Askanas, Valerie

    clinical and pathologic aspects, and basic research potentially relevant to treatment

    (Neurology ; 66,2, Suppl. 1)

    2006  

    Title variant Inclusion-body myositis
    Author's details Valerie Askanas ..., guest ed
    Series title Neurology ; 66,2, Suppl. 1
    Collection
    Language English
    Size S124 S. : Ill., graph. Darst.
    Publisher Lippincott Williams & Wilkins
    Publishing place Hagerstown, Md
    Publishing country United States
    Document type Book
    HBZ-ID HT014684781
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Ui II Zs 153 -66,2,Suppl.1- verfügbar in Königswinter Königswinter

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  2. Book: Inclusion body myositis and myopathies

    Askanas, Valerie

    1998  

    Title variant inclusion-body
    Author's details ed. by Valerie Askanas
    Keywords Myositis, Inclusion Body ; Myositis ; Muskelkrankheit ; Einschlußkörpermyositis
    Subject Myopathie ; Muskelerkrankung ; Myitis ; Muskelentzündung
    Language English
    Size XVIII, 393 S. : Ill., graph. Darst.
    Publisher Cambridge Univ. Press
    Publishing place Cambridge
    Publishing country Great Britain
    Document type Book
    Note Includes index
    HBZ-ID HT009002484
    ISBN 0-521-57105-7 ; 978-0-521-57105-0
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1998 A 6183 order for loan Magazin

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  3. Book: Muscle aging, inclusion body myositis and myopathies

    Askanas, Valerie / Engel, William King

    2012  

    Title variant Muscle aging, inclusion-body myositis and myopathies
    Author's details ed. by Valerie Askanas and W. King Engel
    Keywords Myositis, Inclusion Body / physiopathology ; Aging
    Language English
    Size XII, 250 S. : Ill., graph. Darst., Kt.
    Publisher Wiley-Blackwell
    Publishing place Oxford u.a.
    Publishing country Great Britain
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT017129985
    ISBN 978-1-4051-9646-8 ; 1-4051-9646-7
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2012 A 788 order for loan Magazin

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  4. Book ; Online: Muscle aging

    Askanas, Valerie / Engel, King

    inclusion-body myositis and myopathies

    2012  

    Author's details edited by Valerie Askanas and King Engel
    MeSH term(s) Aging ; Myositis, Inclusion Body/physiopathology
    Keywords Aging ; Myositis
    Language English
    Size Online-Ressource
    Publisher Wiley-Blackwell
    Publishing place Oxford
    Document type Book ; Online
    Note Includes bibliographical references and index
    ISBN 1283408759 ; 9781405196468 ; 1444398288 ; 1444398318 ; 9781283408752 ; 9781405196468 ; 9781444398281 ; 9781444398311 ; 1405196467 ; 1405196467
    DOI 10.1002/9781444398311
    Database Former special subject collection: coastal and deep sea fishing

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  5. Article: Update on neuromuscular diseases: Pathology and molecular pathogenesis.

    Askanas, Valerie / King Engel, William

    Biochimica et biophysica acta

    2015  Volume 1852, Issue 4, Page(s) 561–562

    MeSH term(s) Humans ; Neuromuscular Diseases/genetics ; Neuromuscular Diseases/metabolism ; Neuromuscular Diseases/pathology ; Portraits as Topic
    Language English
    Publishing date 2015-04
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2015.01.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: Muscle aging, inclusion-body myositis and myopathies

    Askanas, Valerie / Engel, W. King

    2012  

    Author's details edited by Valerie Askanas and W. King Engel
    MeSH term(s) Myositis, Inclusion Body/physiopathology ; Aging
    Language English
    Size xii, 250 p. :, ill.
    Publisher Wiley-Blackwell
    Publishing place Oxford
    Document type Book
    ISBN 9781405196468 ; 1405196467
    Database Catalogue of the US National Library of Medicine (NLM)

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  7. Article: Sporadic inclusion-body myositis: A degenerative muscle disease associated with aging, impaired muscle protein homeostasis and abnormal mitophagy.

    Askanas, Valerie / Engel, W King / Nogalska, Anna

    Biochimica et biophysica acta

    2015  Volume 1852, Issue 4, Page(s) 633–643

    Abstract: Sporadic inclusion-body myositis (s-IBM) is the most common degenerative muscle disease in which aging appears to be a key risk factor. In this review we focus on several cellular molecular mechanisms responsible for multiprotein aggregation and ... ...

    Abstract Sporadic inclusion-body myositis (s-IBM) is the most common degenerative muscle disease in which aging appears to be a key risk factor. In this review we focus on several cellular molecular mechanisms responsible for multiprotein aggregation and accumulations within s-IBM muscle fibers, and their possible consequences. Those include mechanisms leading to: a) accumulation in the form of aggregates within the muscle fibers, of several proteins, including amyloid-β42 and its oligomers, and phosphorylated tau in the form of paired helical filaments, and we consider their putative detrimental influence; and b) protein misfolding and aggregation, including evidence of abnormal myoproteostasis, such as increased protein transcription, inadequate protein disposal, and abnormal posttranslational modifications of proteins. Pathogenic importance of our recently demonstrated abnormal mitophagy is also discussed. The intriguing phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer and Parkinson's disease patients, the two most common neurodegenerative diseases associated with aging, are also discussed. This article is part of a Special Issue entitled: Neuromuscular Diseases: Pathology and Molecular Pathogenesis.
    MeSH term(s) Aging/metabolism ; Aging/pathology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Animals ; Brain/metabolism ; Brain/pathology ; Humans ; Muscle Fibers, Skeletal/metabolism ; Muscle Fibers, Skeletal/pathology ; Myositis, Inclusion Body/metabolism ; Myositis, Inclusion Body/pathology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Peptide Fragments ; Protein Aggregation, Pathological/metabolism ; Protein Aggregation, Pathological/pathology ; Protein Biosynthesis ; Protein Processing, Post-Translational ; Proteostasis Deficiencies/metabolism ; Proteostasis Deficiencies/mortality
    Chemical Substances Amyloid beta-Peptides ; Peptide Fragments ; amyloid beta-protein (1-42)
    Language English
    Publishing date 2015-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2014.09.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Sporadic inclusion-body myositis: conformational multifactorial ageing-related degenerative muscle disease associated with proteasomal and lysosomal inhibition, endoplasmic reticulum stress, and accumulation of amyloid-β42 oligomers and phosphorylated tau.

    Askanas, Valerie / Engel, W King

    Presse medicale (Paris, France : 1983)

    2011  Volume 40, Issue 4 Pt 2, Page(s) e219–35

    Abstract: The pathogenesis of sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is complex and multifactorial. Both the muscle fiber degeneration and the mononuclear-cell inflammation are components of the s-IBM pathology, ... ...

    Abstract The pathogenesis of sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is complex and multifactorial. Both the muscle fiber degeneration and the mononuclear-cell inflammation are components of the s-IBM pathology, but how each relates to the pathogenesis remains unsettled. We consider that the intramuscle fiber degenerative component plays the primary and the major pathogenic role leading to muscle fiber destruction and clinical weakness. In this article we review the newest research advances that provide a better understanding of the s-IBM pathogenesis. Cellular abnormalities occurring in s-IBM muscle fibers are discussed, including: several proteins that are accumulated in the form of aggregates within muscle fibers, including amyloid-β42 and its oligomers, and phosphorylated tau in the form of paired helical filaments, and we consider their putative detrimental influence; cellular mechanisms leading to protein misfolding and aggregation, including evidence of their inadequate disposal; pathogenic importance of endoplasmic reticulum stress and the unfolded protein response demonstrated in s-IBM muscle fibers; and decreased deacetylase activity of SIRT1. All these factors are combined with, and perhaps provoked by, an ageing intracellular milieu. Also discussed are the intriguing phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer and Parkinson's disease patients, the two most common neurodegenerative diseases associated with ageing. Muscle biopsy diagnostic criteria are also described and illustrated.
    MeSH term(s) Age Factors ; Amyloid beta-Peptides/metabolism ; Autophagy/physiology ; Biopsy ; Endoplasmic Reticulum/pathology ; Endoplasmic Reticulum/physiology ; Humans ; Lysosomes/metabolism ; Lysosomes/pathology ; Microscopy, Electron ; Muscle Fibers, Skeletal/pathology ; Muscle Fibers, Skeletal/physiology ; Muscles/pathology ; Muscles/physiopathology ; Myositis, Inclusion Body/pathology ; Myositis, Inclusion Body/physiopathology ; Myostatin/metabolism ; Peptide Fragments/metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex/metabolism ; Protein Conformation ; Proteostasis Deficiencies/pathology ; Proteostasis Deficiencies/physiopathology ; Sirtuin 1/metabolism ; Ubiquitin-Protein Ligases/metabolism ; alpha-Synuclein/metabolism ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; MAPT protein, human ; Myostatin ; Peptide Fragments ; alpha-Synuclein ; amyloid beta-protein (1-42) ; tau Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
    Language English
    Publishing date 2011-04
    Publishing country France
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 120943-7
    ISSN 2213-0276 ; 0032-7867 ; 0755-4982 ; 0301-1518
    ISSN (online) 2213-0276
    ISSN 0032-7867 ; 0755-4982 ; 0301-1518
    DOI 10.1016/j.lpm.2010.11.024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains.

    Askanas, Valerie / Engel, W King

    Acta neuropathologica

    2008  Volume 116, Issue 6, Page(s) 583–595

    Abstract: Sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is of unknown cause and lacks successful treatment. Here we summarize diagnostic criteria and discuss our current understanding of the steps in the pathogenic ... ...

    Abstract Sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is of unknown cause and lacks successful treatment. Here we summarize diagnostic criteria and discuss our current understanding of the steps in the pathogenic cascade. While it is agreed that both degeneration and mononuclear-cell inflammation are components of the s-IBM pathology, how each relates to the pathogenesis remains unsettled. We suggest that the intra-muscle-fiber degenerative component plays the primary role, leading to muscle-fiber destruction and clinical weakness, since anti-inflammatory treatments are not of sustained benefit. We discuss possible treatment strategies aimed toward ameliorating a degenerative component, for example, lithium and resveratrol. Also discussed are the intriguing phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer and Parkinson's diseases, the most common neurodegenerative diseases associated with aging. Similarities include, in the respective tissues, cellular aging, mitochondrial abnormalities, oxidative and endoplasmic-reticulum stresses, proteasome inhibition and multiprotein aggregates.
    MeSH term(s) Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Brain/pathology ; Brain/physiopathology ; Humans ; Muscle Fibers, Skeletal/pathology ; Muscle Weakness/physiopathology ; Myositis, Inclusion Body/diagnosis ; Myositis, Inclusion Body/physiopathology ; Nerve Degeneration/physiopathology ; Parkinson Disease/pathology ; Parkinson Disease/physiopathology
    Language English
    Publishing date 2008-12
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-008-0449-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Pathogenic considerations in sporadic inclusion-body myositis, a degenerative muscle disease associated with aging and abnormalities of myoproteostasis.

    Askanas, Valerie / Engel, W King / Nogalska, Anna

    Journal of neuropathology and experimental neurology

    2012  Volume 71, Issue 8, Page(s) 680–693

    Abstract: The pathogenesis of sporadic inclusion-body myositis (s-IBM) is complex; it involves multidimensional pathways and the most critical issues are still unresolved. The onset of muscle fiber damage is age related and the disease is slowly, but inexorably, ... ...

    Abstract The pathogenesis of sporadic inclusion-body myositis (s-IBM) is complex; it involves multidimensional pathways and the most critical issues are still unresolved. The onset of muscle fiber damage is age related and the disease is slowly, but inexorably, progressive. Muscle fiber degeneration and mononuclear cell inflammation are major components of s-IBM pathology, but which is precedent and how they interrelate is not known. There is growing evidence that aging of the muscle fiber associated with intramyofiber accumulation of conformationally modified proteins plays a primary pathogenic role leading to muscle fiber destruction. Here, we review the presumably most important known molecular abnormalities that occur in s-IBM myofibers and that likely contribute to s-IBM pathogenesis. Abnormal accumulation within the fibers of multiprotein aggregates (several of which are congophilic and, therefore, generically called "amyloid") may result from increased transcription of several proteins, their abnormal posttranslational modifications and misfolding, and inadequate protein disposal, that is, abnormal "myoproteostasis," which is combined with and may be provoked or abetted by an aging intracellular milieu. The potential cytotoxicity of accumulated amyloid β protein (Aβ42) and its oligomers, phosphorylated tau in the form of paired helical filaments and α-synuclein, and the putative pathogenic role and cause of the mitochondrial abnormalities and oxidative stress are reviewed. On the basis of our experimental evidence, potential interventions in the complex, interwoven pathogenic cascade of s-IBM are suggested.
    MeSH term(s) Aging/pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/biosynthesis ; Amyloid beta-Protein Precursor/genetics ; Autophagy ; Biopsy ; Humans ; Lithium Compounds/therapeutic use ; Mitochondria, Muscle/metabolism ; Muscle Fibers, Skeletal/pathology ; Muscle Proteins/metabolism ; Muscle, Skeletal/pathology ; Myositis, Inclusion Body/diagnosis ; Myositis, Inclusion Body/drug therapy ; Myositis, Inclusion Body/metabolism ; Myositis, Inclusion Body/pathology ; Peptide Fragments/metabolism ; Phenylbutyrates/therapeutic use ; Polyphenols/therapeutic use ; Proteasome Endopeptidase Complex/metabolism ; Proteostasis Deficiencies/diagnosis ; Proteostasis Deficiencies/drug therapy ; Proteostasis Deficiencies/metabolism ; Proteostasis Deficiencies/pathology ; alpha-Synuclein/metabolism ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Lithium Compounds ; Muscle Proteins ; Peptide Fragments ; Phenylbutyrates ; Polyphenols ; alpha-Synuclein ; amyloid beta-protein (1-42) ; tau Proteins ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; ATP dependent 26S protease (EC 3.4.99.-)
    Language English
    Publishing date 2012-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3088-0
    ISSN 1554-6578 ; 0022-3069
    ISSN (online) 1554-6578
    ISSN 0022-3069
    DOI 10.1097/NEN.0b013e31826183c8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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