Publications by authors named "A Quiroga-Varela"

Background And Objectives: The role of the complement system in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is not completely understood, and studies exploring its potential utility for diagnosis and prognosis are lacking. We aimed to investigate the value of complement factors (CFs) as diagnostic and prognostic biomarkers in patients with MOGAD.

Methods: Multicentric retrospective cohort study including patients with MOGAD, multiple sclerosis (MS) and aquaporin-4 seropositive neuromyelitis optica spectrum disorder (AQP4-NMOSD) with available paired serum and CSF samples.

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Immunohistochemical studies have identified complement component C1q in MS lesions. We aimed to compare serum (sC1q) and CSF (csfC1q) levels in a large cohort of MS patients (pwMS) (n = 222) with those of healthy controls (HC, n = 52), individuals with other immune (IND, n = 14), and non-immune neurological disorders (nIND, n = 15), and to analyze their correlation with other biomarkers. pwMS were divided into three series based on their origin.

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Article Synopsis
  • - The study explored how serum neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) levels could predict worsening disability in multiple sclerosis (MS), enrolling 725 patients across 13 European hospitals from 1994 to 2023.
  • - Higher levels of sNfL were significantly associated with increased risks of relapse-associated worsening (RAW), progression independent of relapse activity (PIRA), and reaching an Expanded Disability Status Scale (EDSS) score of 3, while elevated sGFAP levels were linked to a higher risk of reaching the EDSS score.
  • - Combining both sNfL and sGFAP levels indicated that low values represented low risk for worsening
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Background: Our objective was to explore various biomarkers for predicting suboptimal responses to disease-modifying treatments (DMTs) in patients with MS (pwMS).

Methods: We conducted a longitudinal, bicentric study with pwMS stratified based on their DMTs responses. Treatment failure (TF) was defined as the onset of a second relapse, presence of two or more T2 new lesions, or disability progression independent of relapse during the follow-up period.

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Background: Calcitriol, the active form of vitamin D (also known as 1,25-dihydroxycholecalciferol), improves the phenotype and increases frataxin levels in cell models of Friedreich ataxia (FRDA).

Objectives: Based on these results, we aimed measuring the effects of a calcitriol dose of 0.25 mcg/24h in the neurological function and frataxin levels when administered to FRDA patients for a year.

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