MS Virtual 2020: Biomarkers


It’s that time of the year again, ECTRIMS in conjunction with its American counterpart, ACTRIMS will now be featured as a virtual conference in the coronavirus era. The program is more streamlined than before, running between Fri, Sep 11 – Sun, Sep 13, 2020.

This year, my focus will be again be on the biomarkers session (Fri, Sep 11) eager to see what’s new and what’s not (so) new.

PS03.02 – MRI Phenotypes and miRNA Signatures in MS

Authors: C. Hemond, B. Healy, S. Tauhid, M. Mazzola, F. Quintana, R. Gandhi, H. Weiner, R. Bakshi

miRNAs effectively silence gene expression.

MicroRNAs (miRNAs) are small, noncoding RNAs (genetic material) that bind to non-translated regions of messenger RNAs (mRNA), ultimately affecting protein generation. Dysregulation of these mRNAs have been linked to autoimmunity. In essence miRNAs can regulate cellular function, and the group here want to check whether there are distinct signatures that correlate with specific changes on MRI.

An important limitation of miRNAs is their stability, and not enough is known about their evolution with the disease from onset to end.

PS03.03 – Biomarkers of neurodegeneration, in particular Tau protein, may predict early disability in Multiple Sclerosis patients.

Authors: E. Virgilio, D. Vecchio, I. Crespi, P. Naldi, R. Cantello, U. Dianzani, C. Comi

Tau like neurofilaments are found in neurones and released during damage. Tau has a niche in neurology as a diagnostic biomarker in Alzheimer’s disease. In MS, findings have been varied sometimes elevated in MS but other times unremarkable. There is even a controversial publication where Tau levels in the cerebrospinal fluid decreased over the course of the disease, reflecting a reduction in neuronal quantity rather than damage. I wander what the findings from this study will be?

PS03.04 – Evidence for infection triggering mechanism in blood transcriptional profile of Radiologically isolated syndrome

Authors: M. Golan, R. Zilkha-Falb, P. Sonis, D. Magalashvili, M. Dolev, S. Menascu, A. Achiron

Radiologically isolated syndrome (RIS) became an entity in demyelinating disorders as more brain MRI’s were performed. RIS defines a cohort of individuals with MRI abnormalities in the absence of symptoms. As an entity RIS cases have a certain degree of risk of developing MS. Epstein-Bar virus (glandular fever) is a risk factor for conversion of the first demyelinating event (clinically isolated syndrome, CIS) converting to MS. It would be interesting to see if the same occurs with RIS.

PS03.05 – Serum glial fibrillary acidic protein, but not S100B or neurofilament light chain predicts future relapses in neuromyelitis optica spectrum disorders

Authors: M. Watanabe, N. Isobe, T. Matsushita, A. Maceski, Y. Nakamura, K. Masaki, J. Kira, D. Leppert, J. Kuhle

Neuromyelitis optica (NMO) is a different entity to that of MS and presentations are clinically more severe with greater levels of morbidity. One of the defining features of NMO is a longitudinally extensive spinal cord inflammation:

Current concept of neuromyelitis optica (NMO) and NMO spectrum disorders |  Journal of Neurology, Neurosurgery & Psychiatry
Radiological findings in neuromyelitis optica (NMO). (A) T2 saggittal MRI of spinal cord in a patient with myelitis and intractable vomiting demonstrates a longitudinal lesion extending from the upper thoracic cord to the medulla (arrows). (B) T1 axial MRI, postadministration of gadolinium in a patient with bilateral optic neuritis demonstrates enhancement of bilateral optic nerves and optic chiasm. (C) T2 fuid attenuation recovery (FLAIR) axial MRI of brain demonstrates signal abnormality (arrow) in the aquaporin-4-rich peri-IIIrd-ventricular diencephalon. (D) T1 axial MRI, postadministration of gadolinium demonstrates multiple areas of patchy enhancement with blurred margin in the adjacent regions (‘cloud-like enhancement’). (E) T2 FLAIR axial MRI demonstrates diffuse cerebral white matter abnormalities suspected in a boy initially suspected to have acute demyelinating encephalomyelitis (ADEM), but who ultimately had a relapsing course, and was found to be NMO-IgG positive. From Lippincott Willliams 2008 (A and B); American Medical Association 2006 and 2008, (C and E). Wiley publishers, 2009 (D).

The underlying pathology in NMO is damage to astrocytes leading to blood brain barrier dysfunction. GFAP and S100B are biomarkers of astroglial dysfunction and combined with neurofilaments (a biomarker of neuroaxonal damage) may be prognostic biomarkers for future disease activity.

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Neuro Doc Gnanapavan




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