Bri2-23 is a potential cerebrospinal fluid biomarker in multiple sclerosis

Harris, Violaine K.; Diamanduros, Andrew; Good, Pamela; Zakin, Elina; Chalivendra, Varun; Sadiq, Saud

doi:10.1016/j.nbd.2010.06.007

Cited by 29 publications

(37 citation statements)

References 28 publications

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“…Neuropsin is mainly engaged in the early stage of LTP and in the process of synaptogenesis (Ziemiańska et al 2012), while its deficiency reduces the seizure threshold (Davies et al 2001). Decreased expression of hNP has been confirmed not only in association with deteriorated cognitive functioning, but also in the people affected by brain dysfunctions (among others suffering from multiple sclerosis, SM) (Dutra et al 2013, Harris et al 2010). …”

Section: Introductionmentioning

confidence: 90%

Human Neuropsin Gene in Depression

et al. 2017

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Section: Introductionmentioning

confidence: 90%

Human Neuropsin Gene in Depression

et al. 2017

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“…CSF levels of MBP correlate with active myelin breakdown, but are not specific to MS, and decline in concert with clinical recovery and disappearance of gadolinium enhancement after treatment with methylprednisolone [132,133]. CSF levels of the transmembrane neuronal protein Bri2-23 are specifically decreased in SPMS patients and correlate with clinical measures of cerebellar and cognitive function [134]. CSF levels of Fetuin-A, an immunoregulatory protease inhibitor, appear to be specifically elevated in active secondary progressive (but not relapsing remitting or primary progressive) MS [134].…”

Section: Csf Biomarkersmentioning

confidence: 97%

“…CSF levels of the transmembrane neuronal protein Bri2-23 are specifically decreased in SPMS patients and correlate with clinical measures of cerebellar and cognitive function [134]. CSF levels of Fetuin-A, an immunoregulatory protease inhibitor, appear to be specifically elevated in active secondary progressive (but not relapsing remitting or primary progressive) MS [134]. Though initially reported to be remarkably specific for MS, the presence of soluble Nogo-A, an inhibitor of neuronal axon outgrowth, was later refuted to be a useful CSF biomarker of MS [135,136].…”

Section: Csf Biomarkersmentioning

confidence: 98%

Biomarkers of disease activity in multiple sclerosis

Graber

Dhib‐Jalbut²

2011

Journal of the Neurological Sciences

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“…Though many of the candidate biomarkers have been validated independently, their clinical utility remains unclear. One exception is fetuin-A (alpha-2-HS-glycoprotein), a secreted glycoprotein originally found during a proteomic analysis of CSF from patients with MS and disease controls [23]. Altered levels of fetuin-A in CSF were associated with early conversion to RRMS [24, 25].…”

Section: Candidate Biomarkers Of Therapeutic Responsementioning

confidence: 99%

Biomarkers of Therapeutic Response in Multiple Sclerosis: Current Status

Harris

Sadiq

2014

Mol Diagn Ther

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Multiple sclerosis (MS) is an autoimmune disease of unknown cause, in which chronic inflammation drives multifocal demyelination of axons in both white and gray matter in the CNS. The pathological course of the disease is heterogeneous and involves an early, predominantly inflammatory demyelinating disease phase of relapsing–remitting MS (RRMS), which, over a variable period of time, evolves into a progressively degenerative stage associated with axonal loss and scar formation, causing physical and cognitive disability. For patients with RRMS, there is a growing arsenal of disease-modifying agents (DMAs), with varying degrees of efficacy, as defined by reduced relapse rates, improved magnetic resonance imaging outcomes, and preservation of neurological function. Establishment of personalized treatment plans remains one of the biggest challenges in therapeutic decision-making in MS because the disease prognosis and individual therapeutic outcomes are extremely difficult to predict. Current research is aimed at discovery and validation of biomarkers that reliably measure disease progression and effective therapeutic intervention. Individual biomarker candidates with evident clinical utility are highlighted in this review and include neutralizing autoantibodies against DMAs, fetuin-A, osteopontin, isoprostanes, chemokine (C-X-C motif) ligand 13 (CXCL13), neurofilament light and heavy, and chitinase 3-like protein. In addition, application of more advanced screening technologies has opened up new categories of biomarkers that move beyond detection of individual soluble proteins, including gene expression and autoantibody arrays, microRNAs, and circulating microvesicles/exosomes. Development of clinically useful biomarkers in MS will not only shape the practice of personalized medicine but will also serve as surrogate markers to enable investigation of innovative treatments within clinical trials that are less costly, are of shorter duration, and have more certainty of outcomes.

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Bri2-23 is a potential cerebrospinal fluid biomarker in multiple sclerosis

Cited by 29 publications

References 28 publications

Human Neuropsin Gene in Depression

Human Neuropsin Gene in Depression

Biomarkers of disease activity in multiple sclerosis

Biomarkers of Therapeutic Response in Multiple Sclerosis: Current Status

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