Literature DB >> 26552061

BACE-1, PS-1 and sAPPβ Levels Are Increased in Plasma from Sporadic Inclusion Body Myositis Patients: Surrogate Biomarkers among Inflammatory Myopathies.

Marc Catalán-García1, Glòria Garrabou1, Constanza Morén1, Mariona Guitart-Mampel1, Ingrid Gonzalez-Casacuberta1, Adriana Hernando1, Jose Miquel Gallego-Escuredo2, Dèlia Yubero3, Francesc Villarroya2, Raquel Montero3, Albert Selva O-Callaghan4, Francesc Cardellach1, Josep Maria Grau1.   

Abstract

Sporadic inclusion body myositis (sIBM) is a rare disease that is difficult to diagnose. Muscle biopsy provides three prominent pathological findings: inflammation, mitochondrial abnormalities and fibber degeneration, represented by the accumulation of protein depots constituted by β-amyloid peptide, among others. We aim to perform a screening in plasma of circulating molecules related to the putative etiopathogenesis of sIBM to determine potential surrogate biomarkers for diagnosis. Plasma from 21 sIBM patients and 20 age- and gender-paired healthy controls were collected and stored at -80°C. An additional population of patients with non-sIBM inflammatory myopathies was also included (nine patients with dermatomyositis and five with polymyositis). Circulating levels of inflammatory cytokines (interleukin [IL]-6 and tumor necrosis factor [TNF]-α), mitochondrial-related molecules (free plasmatic mitochondrial DNA [mtDNA], fibroblast growth factor-21 [FGF-21] and coenzyme-Q10 [CoQ]) and amyloidogenic-related molecules (beta-secretase-1 [BACE-1], presenilin-1 [PS-1], and soluble Aβ precursor protein [sAPPβ]) were assessed with magnetic bead-based assays, real-time polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA) and high-pressure liquid chromatography (HPLC). Despite remarkable trends toward altered plasmatic expression of inflammatory and mitochondrial molecules (increased IL-6, TNF-α, circulating mtDNA and FGF-21 levels and decreased content in CoQ), only amyloidogenic degenerative markers including BACE-1, PS-1 and sAPPβ levels were significantly increased in plasma from sIBM patients compared with controls and other patients with non-sIBM inflammatory myopathies (p < 0.05). Inflammatory, mitochondrial and amyloidogenic degeneration markers are altered in plasma of sIBM patients confirming their etiopathological implication in the disease. Sensitivity and specificity analysis show that BACE-1, PS-1 and sAPPβ represent a good predictive noninvasive tool for the diagnosis of sIBM, especially in distinguishing this disease from polymyositis.

Entities:  

Year:  2015        PMID: 26552061      PMCID: PMC4818257          DOI: 10.2119/molmed.2015.00168

Source DB:  PubMed          Journal:  Mol Med        ISSN: 1076-1551            Impact factor:   6.354


  39 in total

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Authors:  Jessica E Hoogendijk; Anthony A Amato; Bryan R Lecky; Ernest H Choy; Ingrid E Lundberg; Michael R Rose; Jiri Vencovsky; Marianne de Visser; Richard A Hughes
Journal:  Neuromuscul Disord       Date:  2004-05       Impact factor: 4.296

2.  Increased BACE1 mRNA and noncoding BACE1-antisense transcript in sporadic inclusion-body myositis muscle fibers--possibly caused by endoplasmic reticulum stress.

Authors:  Anna Nogalska; W King Engel; Valerie Askanas
Journal:  Neurosci Lett       Date:  2010-03-15       Impact factor: 3.046

Review 3.  Inclusion-body myositis and Alzheimer disease: two sides of the same coin, or different currencies altogether?

Authors:  M Paul Murphy; Todd E Golde
Journal:  Neurology       Date:  2006-01-24       Impact factor: 9.910

Review 4.  Inclusion body myositis: diagnosis, pathogenesis, and treatment options.

Authors:  Guillermo E Solorzano; Lawrence H Phillips
Journal:  Rheum Dis Clin North Am       Date:  2011-05       Impact factor: 2.670

Review 5.  Inclusion body myositis and myopathies.

Authors:  R C Griggs; V Askanas; S DiMauro; A Engel; G Karpati; J R Mendell; L P Rowland
Journal:  Ann Neurol       Date:  1995-11       Impact factor: 10.422

6.  Inclusion body myositis presenting as treatment-resistant polymyositis.

Authors:  L H Calabrese; H Mitsumoto; S M Chou
Journal:  Arthritis Rheum       Date:  1987-04

7.  Inclusion body myositis in Alzheimer's disease.

Authors:  P M Roos; O Vesterberg; M Nordberg
Journal:  Acta Neurol Scand       Date:  2010-12-22       Impact factor: 3.209

8.  A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities.

Authors:  Fieke M Cox; Maarten J Titulaer; Jacob K Sont; Axel R Wintzen; Jan J G M Verschuuren; Umesh A Badrising
Journal:  Brain       Date:  2011-09-09       Impact factor: 13.501

9.  Long-term observational study of sporadic inclusion body myositis.

Authors:  Olivier Benveniste; Marguerite Guiguet; Jane Freebody; Odile Dubourg; Waney Squier; Thierry Maisonobe; Tanya Stojkovic; Maria Isabel Leite; Yves Allenbach; Serge Herson; Stefen Brady; Bruno Eymard; David Hilton-Jones
Journal:  Brain       Date:  2011-10-12       Impact factor: 13.501

Review 10.  Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken.

Authors:  Olivier Benveniste; Werner Stenzel; David Hilton-Jones; Marco Sandri; Olivier Boyer; Baziel G M van Engelen
Journal:  Acta Neuropathol       Date:  2015-01-13       Impact factor: 17.088

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  5 in total

Review 1.  Update on Inclusion Body Myositis.

Authors:  Duaa Jabari; V V Vedanarayanan; Richard J Barohn; Mazen M Dimachkie
Journal:  Curr Rheumatol Rep       Date:  2018-06-28       Impact factor: 4.592

Review 2.  Inclusion Body Myositis: Update on Pathogenesis and Treatment.

Authors:  Elie Naddaf; Richard J Barohn; Mazen M Dimachkie
Journal:  Neurotherapeutics       Date:  2018-10       Impact factor: 7.620

Review 3.  Immune and myodegenerative pathomechanisms in inclusion body myositis.

Authors:  Christian W Keller; Jens Schmidt; Jan D Lünemann
Journal:  Ann Clin Transl Neurol       Date:  2017-05-16       Impact factor: 4.511

4.  Mitochondrial dysfunction underlying sporadic inclusion body myositis is ameliorated by the mitochondrial homing drug MA-5.

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Journal:  PLoS One       Date:  2020-12-02       Impact factor: 3.240

5.  Peripheral Aβ acts as a negative modulator of insulin secretion.

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Journal:  Proc Natl Acad Sci U S A       Date:  2022-03-15       Impact factor: 12.779

  5 in total

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