Cerebrospinal fluid complement system biomarkers in demyelinating disease. 2020

Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
Systems Immunity University Research Institute, Cardiff University, Cardiff, UK.

Multiple sclerosis (MS) can be difficult to differentiate from other demyelinating diseases, notably neuromyelitis optica spectrum disorder (NMOSD). We previously showed that NMOSD is distinguished from MS by plasma complement biomarkers. Here, we measure cerebrospinal fluid (CSF) complement proteins in MS, NMOSD and clinically isolated syndrome (CIS), a neurological episode that may presage MS, to test whether these distinguish NMOSD from MS and CIS. CSF (53 MS, 17 CIS, 11 NMOSD, 35 controls) was obtained; complement proteins (C4, C3, C5, C9, C1, C1q, Factor B (FB)), regulators (Factor I (FI), Factor H (FH), FH-Related Proteins 1, 2 and 5 (FHR125), C1 Inhibitor (C1INH), Properdin) and activation products (terminal complement complex (TCC), iC3b) were quantified by ELISA and results expressed relative to CSF total protein (μg/mg). Compared to control CSF, (1) levels of C4, C1INH and Properdin were elevated in MS; (2) TCC, iC3b, FI and FHR125 were increased in CIS; and (3) all complement biomarkers except TCC, FHR125, Properdin and C5 were higher in NMOSD CSF. A statistical model comprising six analytes (C3, C9, FB, C1q, FI, Properdin) plus age/gender optimally differentiated MS from NMOSD.

UI MeSH Term Description Entries
D009103 Multiple Sclerosis An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903) MS (Multiple Sclerosis),Multiple Sclerosis, Acute Fulminating,Sclerosis, Disseminated,Disseminated Sclerosis,Sclerosis, Multiple
D009471 Neuromyelitis Optica A syndrome characterized by acute OPTIC NEURITIS; MYELITIS, TRANSVERSE; demyelinating and/or necrotizing lesions in the OPTIC NERVES and SPINAL CORD; and presence of specific autoantibodies to AQUAPORIN 4. Devic Disease,Devic's Neuromyelitis Optica,Devic Neuromyelitis Optica,Devic Syndrome,Devic's Disease,Devic's Syndrome,NMO Spectrum Disorder,Neuromyelitis Optica (NMO) Spectrum Disorder,Neuromyelitis Optica (NMO) Spectrum Disorders,Neuromyelitis Optica Spectrum Disorder,Neuromyelitis Optica Spectrum Disorders,Devic Neuromyelitis Opticas,Devics Disease,Devics Neuromyelitis Optica,Devics Syndrome,Disease, Devic,Disease, Devic's,NMO Spectrum Disorders,Neuromyelitis Optica, Devic,Neuromyelitis Optica, Devic's,Neuromyelitis Opticas, Devic,Syndrome, Devic,Syndrome, Devic's
D003165 Complement System Proteins Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY). Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D015415 Biomarkers Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, ENVIRONMENTAL EXPOSURE and its effects, disease diagnosis; METABOLIC PROCESSES; SUBSTANCE ABUSE; PREGNANCY; cell line development; EPIDEMIOLOGIC STUDIES; etc. Biochemical Markers,Biological Markers,Biomarker,Clinical Markers,Immunologic Markers,Laboratory Markers,Markers, Biochemical,Markers, Biological,Markers, Clinical,Markers, Immunologic,Markers, Laboratory,Markers, Serum,Markers, Surrogate,Markers, Viral,Serum Markers,Surrogate Markers,Viral Markers,Biochemical Marker,Biologic Marker,Biologic Markers,Clinical Marker,Immune Marker,Immune Markers,Immunologic Marker,Laboratory Marker,Marker, Biochemical,Marker, Biological,Marker, Clinical,Marker, Immunologic,Marker, Laboratory,Marker, Serum,Marker, Surrogate,Serum Marker,Surrogate End Point,Surrogate End Points,Surrogate Endpoint,Surrogate Endpoints,Surrogate Marker,Viral Marker,Biological Marker,End Point, Surrogate,End Points, Surrogate,Endpoint, Surrogate,Endpoints, Surrogate,Marker, Biologic,Marker, Immune,Marker, Viral,Markers, Biologic,Markers, Immune
D015938 Complement Membrane Attack Complex A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC. Complement Complex C5b-9,Membrane Attack Complex,C 5b-9,C5b-8-poly-C9,C5b-9,Cytolytic Terminal Complement Complex,Terminal Complement Complex,C5b 8 poly C9,Complement Complex C5b 9,Complement Complex, Terminal,Complex, Terminal Complement

Related Publications

Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
November 1986, Neurology,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
January 1980, Journal of neurology,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
May 2019, Multiple sclerosis and related disorders,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
March 2013, Nature reviews. Neurology,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
April 1980, Journal of the neurological sciences,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
January 2009, Journal of Alzheimer's disease : JAD,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
January 2016, Journal of Huntington's disease,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
February 2010, Biomarkers in medicine,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
April 2014, Neuroscience bulletin,
Wioleta Milena Zelek, and Dina Fathalla, and Angharad Morgan, and Samuel Touchard, and Samantha Loveless, and Emma Tallantyre, and Neil P Robertson, and B Paul Morgan
April 1977, The New England journal of medicine,
Copied contents to your clipboard!