Valerie Askanas

Summary

Affiliation: University of Southern California
Country: USA

Publications

  1. ncbi request reprint BACE1 and BACE2 in pathologic and normal human muscle
    Gaetano Vattemi
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles 90017 1912, USA
    Exp Neurol 179:150-8. 2003
  2. ncbi request reprint Cystatin C colocalizes with amyloid-beta and coimmunoprecipitates with amyloid-beta precursor protein in sporadic inclusion-body myositis muscles
    Gaetano Vattemi
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    J Neurochem 85:1539-46. 2003
  3. pmc Endoplasmic reticulum stress and unfolded protein response in inclusion body myositis muscle
    Gaetano Vattemi
    Department of Neurology, University of Southern California Neuromuscular Center, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Am J Pathol 164:1-7. 2004
  4. doi request reprint Pathogenic considerations in sporadic inclusion-body myositis, a degenerative muscle disease associated with aging and abnormalities of myoproteostasis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    J Neuropathol Exp Neurol 71:680-93. 2012
  5. ncbi request reprint Molecular pathology and pathogenesis of inclusion-body myositis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Microsc Res Tech 67:114-20. 2005
  6. ncbi request reprint Inclusion-body myositis, a multifactorial muscle disease associated with aging: current concepts of pathogenesis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Curr Opin Rheumatol 19:550-9. 2007
  7. pmc Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains
    Valerie Askanas
    Department of Neurology, USC Neuromuscular Center, Good Samaritan Hospital, University of Southern California Keck School of Medicine, 637 South Lucas Avenue, Los Angeles, CA 90017 1912, USA
    Acta Neuropathol 116:583-95. 2008
  8. doi request reprint Inclusion body myositis: a degenerative muscle disease associated with intra-muscle fiber multi-protein aggregates, proteasome inhibition, endoplasmic reticulum stress and decreased lysosomal degradation
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Brain Pathol 19:493-506. 2009
  9. doi request reprint 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
    Valerie Askanas
    University of Southern California Keck School of Medicine, Good Samaritan Hospital, USC Neuromuscular Centre, Department of Neurology, Los Angeles, CA 90017, USA
    Presse Med 40:e219-35. 2011
  10. ncbi request reprint Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA, USA
    Neurology 66:S39-48. 2006

Collaborators

Detail Information

Publications35

  1. ncbi request reprint BACE1 and BACE2 in pathologic and normal human muscle
    Gaetano Vattemi
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles 90017 1912, USA
    Exp Neurol 179:150-8. 2003
    ..Accordingly, BACE1 and BACE2 participate in normal and abnormal processes of human muscle, suggesting that their functions are broader than previously thought...
  2. ncbi request reprint Cystatin C colocalizes with amyloid-beta and coimmunoprecipitates with amyloid-beta precursor protein in sporadic inclusion-body myositis muscles
    Gaetano Vattemi
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    J Neurochem 85:1539-46. 2003
    ..Our studies (i) demonstrate for the first time that CC physically associates with A beta PP, and (ii) suggest that CC may play a novel role in the s-IBM pathogenesis, possibly by influencing A beta PP processing and A beta deposition...
  3. pmc Endoplasmic reticulum stress and unfolded protein response in inclusion body myositis muscle
    Gaetano Vattemi
    Department of Neurology, University of Southern California Neuromuscular Center, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Am J Pathol 164:1-7. 2004
    ....
  4. doi request reprint Pathogenic considerations in sporadic inclusion-body myositis, a degenerative muscle disease associated with aging and abnormalities of myoproteostasis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    J Neuropathol Exp Neurol 71:680-93. 2012
    ..On the basis of our experimental evidence, potential interventions in the complex, interwoven pathogenic cascade of s-IBM are suggested...
  5. ncbi request reprint Molecular pathology and pathogenesis of inclusion-body myositis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Microsc Res Tech 67:114-20. 2005
    ..Our basic hypothesis is that overexpression of AbetaPP within the aging muscle fibers is an early upstream event causing a subsequent pathogenic cascade...
  6. ncbi request reprint Inclusion-body myositis, a multifactorial muscle disease associated with aging: current concepts of pathogenesis
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Curr Opin Rheumatol 19:550-9. 2007
    ..About 100 papers related to the subject were published in 2006 and the first part of 2007 (we cite only articles most relevant to this review)...
  7. pmc Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains
    Valerie Askanas
    Department of Neurology, USC Neuromuscular Center, Good Samaritan Hospital, University of Southern California Keck School of Medicine, 637 South Lucas Avenue, Los Angeles, CA 90017 1912, USA
    Acta Neuropathol 116:583-95. 2008
    ..Similarities include, in the respective tissues, cellular aging, mitochondrial abnormalities, oxidative and endoplasmic-reticulum stresses, proteasome inhibition and multiprotein aggregates...
  8. doi request reprint Inclusion body myositis: a degenerative muscle disease associated with intra-muscle fiber multi-protein aggregates, proteasome inhibition, endoplasmic reticulum stress and decreased lysosomal degradation
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Brain Pathol 19:493-506. 2009
    ..Together, these appear to lead to the s-IBM-specific vacuolar degeneration, and muscle fiber atrophy, concluding with muscle fiber death...
  9. doi request reprint 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
    Valerie Askanas
    University of Southern California Keck School of Medicine, Good Samaritan Hospital, USC Neuromuscular Centre, Department of Neurology, Los Angeles, CA 90017, USA
    Presse Med 40:e219-35. 2011
    ..Muscle biopsy diagnostic criteria are also described and illustrated...
  10. ncbi request reprint Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA, USA
    Neurology 66:S39-48. 2006
    ....
  11. doi request reprint Amyloid-beta42 is preferentially accumulated in muscle fibers of patients with sporadic inclusion-body myositis
    Gaetano Vattemi
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA, 90017, USA
    Acta Neuropathol 117:569-74. 2009
    ..Thus, in s-IBM muscle fibers, Abeta42 is accumulated more than Abeta40. We suggest that Abeta42 oligomers and their cytotoxicity may play an important role in the s-IBM pathogenesis...
  12. pmc Endoplasmic reticulum stress induces myostatin precursor protein and NF-kappaB in cultured human muscle fibers: relevance to inclusion body myositis
    Anna Nogalska
    Department of Neurology, USC Neuromuscular Center, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S Lucas Avenue, Los Angeles, CA 90017, USA
    Exp Neurol 204:610-8. 2007
    ....
  13. ncbi request reprint Homocysteine-induced endoplasmic reticulum protein (Herp) is up-regulated in sporadic inclusion-body myositis and in endoplasmic reticulum stress-induced cultured human muscle fibers
    Anna Nogalska
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    J Neurochem 96:1491-9. 2006
    ....
  14. doi request reprint p62/SQSTM1 is overexpressed and prominently accumulated in inclusions of sporadic inclusion-body myositis muscle fibers, and can help differentiating it from polymyositis and dermatomyositis
    Anna Nogalska
    Department of Neurology, USC Neuromuscular Center, Good Samaritan Hospital, University of Southern California Keck School of Medicine, Los Angeles, CA 90017 1912, USA
    Acta Neuropathol 118:407-13. 2009
    ....
  15. pmc In AbetaPP-overexpressing cultured human muscle fibers proteasome inhibition enhances phosphorylation of AbetaPP751 and GSK3beta activation: effects mitigated by lithium and apparently relevant to sporadic inclusion-body myositis
    Chiara Terracciano
    Department of Neurology, USC Neuromuscular Center, University of Southern California Keck, School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017, USA
    J Neurochem 112:389-96. 2010
    ..2) In biopsied s-IBM muscle fibers, GSK3beta is significantly activated and AbetaPP is phosphorylated on Thr724. Accordingly, treatment with lithium, or other GSK3beta inhibitors, might benefit s-IBM patients...
  16. ncbi request reprint NOGO is increased and binds to BACE1 in sporadic inclusion-body myositis and in A beta PP-overexpressing cultured human muscle fibers
    Slawomir Wojcik
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S Lucas Ave, Los Angeles, CA 90017 1912, USA
    Acta Neuropathol 114:517-26. 2007
    ..However, the increase of Nogo-B seems insufficient because A beta continues to accumulate and the disease progresses. We propose that manipulations, which increase Nogo-B in s-IBM muscle might offer a new therapeutic opportunity...
  17. ncbi request reprint Inclusion-body myositis and myopathies: different etiologies, possibly similar pathogenic mechanisms
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017, USA
    Curr Opin Neurol 15:525-31. 2002
    ..Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion body myopathies are progressive muscle diseases that lead to severe disability. We discuss recent advances in illuminating their pathogenic mechanism(s)...
  18. doi request reprint Novel demonstration of conformationally modified tau in sporadic inclusion-body myositis muscle fibers
    Anna Nogalska
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S Lucas Ave, Los Angeles, CA 90017 1912, USA
    Neurosci Lett 503:229-33. 2011
    ..This first demonstration of conformational tau in s-IBM, because of its abundance in non-atrophic muscle fibers, suggests that it might play an early role in s-IBM PHFs formation and thus be pathogenically important...
  19. ncbi request reprint Transthyretin Val122Ile, accumulated Abeta, and inclusion-body myositis aspects in cultured muscle
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles 90017 1912, USA
    Neurology 61:257-60. 2003
    ..These abnormalities are never present in normal human CMF. These perturbations were greatly increased after Abeta precursor protein gene transfer. The TTR mutation may be a genetic predisposition factor for the patient's IBM...
  20. ncbi request reprint Unfolding story of inclusion-body myositis and myopathies: role of misfolded proteins, amyloid-beta, cholesterol, and aging
    Valerie Askanas
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    J Child Neurol 18:185-90. 2003
    ..We discuss a potentially very important role of unfolded and/or misfolded proteins as a possible mechanism in the formations of the inclusion bodies and other abnormalities...
  21. ncbi request reprint Proposed pathogenetic cascade of inclusion-body myositis: importance of amyloid-beta, misfolded proteins, predisposing genes, and aging
    Valerie Askanas
    Department of Neurology, University of Southern California, Keck School of Medicine, Good Samaritan Hospital, Los Angeles, California 90017 1912, USA
    Curr Opin Rheumatol 15:737-44. 2003
    ....
  22. pmc AbetaPP-overexpression and proteasome inhibition increase alphaB-crystallin in cultured human muscle: relevance to inclusion-body myositis
    Slawomir Wojcik
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Neuromuscul Disord 16:839-44. 2006
    ..We propose that increased AbetaPP is a stressor increasing alphaBC expression in s-IBM muscle fibers. Determining the consequences of alphaBC association with Abeta oligomers could have clinical therapeutic relevance...
  23. pmc Impaired autophagy in sporadic inclusion-body myositis and in endoplasmic reticulum stress-provoked cultured human muscle fibers
    Anna Nogalska
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Am J Pathol 177:1377-87. 2010
    ..Thus, unblocking protein degradation in s-IBM muscle fibers may be a desirable therapeutic strategy...
  24. ncbi request reprint Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers
    Sławomir Wójcik
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S Lucas Ave, Los Angeles, CA, 90017 1912, USA
    Acta Neuropathol 110:173-7. 2005
    ..Our study suggests that myostatin/myostatin precursor, either alone, or bound to Abeta, may play a novel role in the pathogenesis of s-IBM...
  25. pmc Proteasome inhibition and aggresome formation in sporadic inclusion-body myositis and in amyloid-beta precursor protein-overexpressing cultured human muscle fibers
    Pietro Fratta
    Department of Neurology, USC Neuromuscular Center, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Am J Pathol 167:517-26. 2005
    ..Accordingly, proteasome dysfunction in s-IBM muscle fibers may play a role in accumulation of misfolded, potentially cytotoxic proteins and may be induced by increased intracellular AbetaPP/Abeta...
  26. doi request reprint Activation of the γ-secretase complex and presence of γ-secretase-activating protein may contribute to Aβ42 production in sporadic inclusion-body myositis muscle fibers
    Anna Nogalska
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Neurobiol Dis 48:141-9. 2012
    ..Accordingly, improving lysosomal function might be a therapeutic strategy for s-IBM patients...
  27. doi request reprint Abnormalities of NBR1, a novel autophagy-associated protein, in muscle fibers of sporadic inclusion-body myositis
    Carla D'Agostino
    Department of Neurology, USC Neuromuscular Center, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, 90017 1912, USA
    Acta Neuropathol 122:627-36. 2011
    ..Accordingly, attempts to unblock defective protein degradation might be a therapeutic strategy for s-IBM patients...
  28. pmc Increased BACE1 mRNA and noncoding BACE1-antisense transcript in sporadic inclusion-body myositis muscle fibers--possibly caused by endoplasmic reticulum stress
    Anna Nogalska
    USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA, USA
    Neurosci Lett 474:140-3. 2010
    ..Accordingly, decreasing BACE1 through a targeted downregulation of its regulatory BACE1-AS, or reducing ER stress, might be therapeutic strategies in s-IBM, assuming that it would not impair any normal cellular functions of BACE1...
  29. ncbi request reprint Inclusion-body myositis: clinical, diagnostic, and pathologic aspects
    W King Engel
    The Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA, USA
    Neurology 66:S20-9. 2006
    ..Available treatments are of only slight, temporary benefit for only some s-IBM patients, indicating a desperate need for definitive therapies...
  30. pmc In inclusion-body myositis muscle fibers Parkinson-associated DJ-1 is increased and oxidized
    Chiara Terracciano
    Department of Neurology, USC Neuromuscular Center, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S Lucas Avenue, Los Angeles, CA 90017 1912, USA
    Free Radic Biol Med 45:773-9. 2008
    ..In s-IBM muscle fibers, DJ-1 could be protecting these fibers against oxidative stress, including protection of mitochondria...
  31. doi request reprint Decreased SIRT1 deacetylase activity in sporadic inclusion-body myositis muscle fibers
    Anna Nogalska
    Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017 1912, USA
    Neurobiol Aging 31:1637-48. 2010
    ..Improving SIRT1 action by treatment with known SIRT1 activators might benefit s-IBM patients...
  32. ncbi request reprint Newest pathogenetic considerations in inclusion-body myositis: possible role of amyloid-beta, cholesterol, relation to aging and to Alzheimer's disease
    Valerie Askanas
    University of Southern California Neuromuscular Center, Good Samaritan Hospital, 637 South Lucas Avenue, Los Angeles, CA 90017 1912, USA
    Curr Rheumatol Rep 4:427-33. 2002
    ..The remarkable pathologic similarities between inclusion-body myositis muscle and Alzheimer's disease brain are discussed...
  33. doi request reprint Novel demonstration of amyloid-β oligomers in sporadic inclusion-body myositis muscle fibers
    Anna Nogalska
    Department of Neurology, USC Neuromuscular Center, Good Samaritan Hospital, University of Southern California Keck School of Medicine, Los Angeles, CA 90017 1912, USA
    Acta Neuropathol 120:661-6. 2010
    ..This novel demonstration of Aβ42 oligomers in s-IBM muscle biopsy provides additional evidence that intra-muscle fiber accumulation of Aβ42 oligomers in s-IBM may contribute importantly to s-IBM pathogenic cascade...
  34. ncbi request reprint Unicorns, dragons, polymyositis, and other mythical beasts
    Valerie Askanas
    Neurology 63:403-4; author reply 404. 2004
  35. ncbi request reprint Expression of Nogo-A in human muscle fibers is not specific for amyotrophic lateral sclerosis
    Valerie Askanas
    Ann Neurol 62:676-7; author reply 677. 2007