Researcher:
Vural, Atay

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Atay

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Vural

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Vural, Atay

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2018 - 2019112020 - 202315

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    Frequency of myelin oligodendrocyte glycoprotein antibodies in pediatric onset multiple sclerosis
    (2022) Solmaz, İsmail; Konuşkan, Bahadır; Öncel, İbrahim; Anlar, Banu; Doran, Tansu; Yousefi, Mohammadreza; Vural, Atay; PhD Student; PhD Student; Faculty Member; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; Koç University Hospital; N/A; N/A; 182369
    Background: Myelin oligodendrocyte glycoprotein antibodies (MOG-Ab) are associated with acute demyelinating syndromes and only rarely detected in multiple sclerosis (MS). As MOG-Ab associated disease is common in childhood, we speculated young patients might be more likely to produce MOG-Ab and investigated the frequency of MOG-Ab seropositivity in pediatric onset MS (POMS).Material and methods: Patients who experienced their first acute demyelinating event before age 18 years and were diagnosed with MS during follow-up were included in this single-center study. Patient data were retrieved from clinical records. Serum samples obtained and frozen at clinical visits were analyzed for MOG-Ab by a live cell-based assay (CBA) measuring delta mean fluorescence intensity (MFI) and MFI ratio. The control group consisted of patients referred to pediatric neurology for headache or vertigo and who had no neurological dis-order (n = 48). Another control group consisted of patients with systemic inflammatory disorders systemic lupus erythematosus (n = 17) and juvenile idiopathic arthritis (n = 13) diagnosed in the rheumatology clinic.Results: The patient group (n 1/4 122, F/M: 90/32, mean age 17.8 & PLUSMN; 2.6 years) were initially diagnosed as: MS, 62/122 (50.8%), clinically isolated syndrome, 43/122 (35.2%), radiologically isolated syndrome, 9/122 (7.3%), and acute disseminated encephalomyelitis 8/122 (6.5%). All received the final diagnosis of POMS. Serum was sampled 22.4 & PLUSMN; 29.2 (0-132) months after the first episode. None of the control groups had MOG-Ab positivity while 2/122 (1.6%) POMS cases had MOG-Abs, and a third patient had positive MFI and a MFI ratio slightly below the cut-off. These three patients' initial and final diagnoses were MS, their annualized relapsing rates (ARRs) were 0.4-0.6, and most recent Expanded Disability Status Scale was 0.Conclusion: Low titers of MOG-Ab can be detected in a small number of POMS patients at similar frequency with adult MS. Our POMS cases with MOG-Abs presented brainstem-cerebellar findings or seizures and had low ARR. Further series and longer follow-up will define whether these cases differ significantly from MOG-Ab negative POMS cases.
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    Circulating myelin oligodendrocyte glycoprotein (MOG)-specific B cells stratify patients with serum MOG-antibodies
    (Wiley, 2019) Winklmeier, S.; Schlueter, M.; Spadaro, M.; Thaler, F. S.; Gerhards, R.; Macrini, C.; Mader, S.; Kurne, A.; İnan, B.; Karabudak, R.; Özbay, F. G.; Esendağlı, G.; Hohlfeld, R.; Kuempfel, T.; Meinl, E.; Vural, Atay; Faculty Member; School of Medicine; 182369
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    Association of pyrin mutations and autoinflammation with complex phenotype hidradenitis suppurativa: a case–control study
    (Wiley, 2019) Gündoğdu, M.; Illi, E. Gökpınar; Durmaz, C. D.; Steinmuller-Magin, L.; Kleinhempel, A.; Holdt, L. M.; Ruzicka, T.; Giehl, K. A.; Ruhi, H., I; Boyvat, A.; Vural, Seçil; Vural, Atay; Faculty Member; Faculty Member; School of Medicine; School of Medicine; 189340; 182369
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    Ocrelizumab treatment modulates B-cell regulating factors in multiple sclerosis
    (Lippincott Williams and Wilkins (LWW), 2023) Ho, Samantha; Oswald, Eva; Wong, Hoi Kiu; Yilmaz, Vuslat; Tuezuen, Erdem; Tuerkoglu, Recai; Straub, Tobias; Meinl, Ingrid; Thaler, Franziska; Kuempfel, Tania; Meinl, Edgar; Mader, Simone; Vural, Atay; Faculty Member; School of Medicine; 182369
    Background and Objectives: Antibodies to CD20 efficiently reduce new relapses in multiple sclerosis (MS), and ocrelizumab has been shown to be effective also in primary progressive MS. Although anti-CD20 treatments efficiently deplete B cells in blood, some B cells and CD20(-) plasma cells persist in lymphatic organs and the inflamed CNS; their survival is regulated by the B cell-activating factor (BAFF)/A proliferation-inducing ligand (APRIL) system. The administration of a soluble receptor for BAFF and APRIL, atacicept, unexpectedly worsened MS. Here, we explored the long-term effects of ocrelizumab on immune cell subsets as well as on cytokines and endogenous soluble receptors comprising the BAFF-APRIL system. Methods: We analyzed immune cell subsets and B cell-regulating factors longitudinally for up to 2.5 years in patients with MS treated with ocrelizumab. In a second cohort, we determined B-cell regulatory factors in the CSF before and after ocrelizumab. We quantified the cytokines BAFF and APRIL along with their endogenous soluble receptors soluble B-cell maturation antigen (sBCMA) and soluble transmembrane activator and calcium-modulator and cyclophilin ligand (CAML) interactor (sTACI) using enzyme-linked immunosorbent assays (ELISAs). In addition, we established an in-house ELISA to measure sTACI-BAFF complexes. Results: Ocrelizumab treatment of people with MS persistently depleted B cells and CD20(+) T cells. This treatment enhanced BAFF and reduced the free endogenous soluble receptor and decoy sTACI in both serum and CSF. Levels of sTACI negatively correlated with BAFF levels. Reduction of sTACI was associated with formation of sTACI-BAFF complexes.DiscussionWe describe a novel effect of anti-CD20 therapy on the BAFF-APRIL system, namely reduction of sTACI. Because sTACI is a decoy for APRIL, its reduction may enhance local APRIL activity, thereby promoting regulatory IgA(+) plasma cells and astrocytic interleukin (IL)-10 production. Thus, reducing sTACI might contribute to the beneficial effect of anti-CD20 as exogenous sTACI (atacicept) worsened MS.Classification of EvidenceThis study provides Class IV evidence that endogenous sTACI in blood and CSF is decreased after ocrelizumab treatment.
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    Cerebellar cognitive-affective syndrome preceding ataxia associated with complex extrapyramidal features in a Turkish SCA48 family
    (Springer, 2020) Kaya-Güleç, Zeynep Ece; Genç, Gencer; N/A; Palvadeau, Robin Jerome; Şimşir, Gülşah; Vural, Atay; Çakmak, Özgür Öztop; Aygün, Murat Serhat; Falay, Fikri Okan; Başak, Ayşe Nazlı; Ertan, Fatoş Sibel; Researcher; Master Student; Faculty Member; Faculty Member; Teaching Faculty; Teaching Faculty; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; Graduate School of Sciences and Engineering; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; 182369; 299358; 291692; 246484; 1512; 112829
    SCA48 is a novel spinocerebellar ataxia (SCA) originally and recently characterized by prominent cerebellar cognitive-affective syndrome (CCAS) and late-onset ataxia caused by mutations on the STUB1 gene. Here, we report the first SCA48 case from Turkey with novel clinical features and diffusion tensor imaging (DTI) findings, used for the first time to evaluate a SCA48 patient. A 65-year-old female patient with slowly progressive cerebellar ataxia, cognitive impairment, behavioral changes, and a vertical family history was evaluated. Following the exclusion of repeat expansion ataxias, whole exome sequencing (WES) was performed. Brain magnetic resonance imaging (MRI), including DTI, and single-photon emission computed tomography (SPECT) were used to study the primarily affected tracts and regions. WES revealed the previously reported heterozygous truncating mutation in ubiquitin ligase domain of STUB1 (ENST00000219548:c.823_824delCT, ENSP00000219548:p.L275Dfs*16) leading to a frameshift. Patient's cognitive status was compatible with CCAS. Novel clinical features different from the original report include later onset chorea, dystonia, general slowness of movements, apraxia, and palilalia, some of which have been recently reported in two families with different STUB1 mutations. CCAS is a prominent and often early feature of SCA48 which may be followed years after the onset of the disease by other complex neurological signs and symptoms. DTI may be helpful for demonstrating the cerebello-frontal tracts, involved in CCAS-associated SCA48, the differential diagnosis of which may be challenging especially in its early years.
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    Neurodegeneration of macular ganglion cells and maculo-papillary bundle is present early in radiologically isolated syndrome and reflects brain atrophy
    (Sage Publications Ltd, 2018) Okar, Serhat; Tuncer, Meryem Aslı; Acar, Nazire Pınar; Sayat, Güliz; Kadayıfcılar, Sibel; Karabudak, Rana; Vural, Atay; Faculty Member; School of Medicine; 182369
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    Myelin oligodendrocyte glycoprotein antibody associated central nervous system demyelinating disease: a tertiary center experience from Turkey
    (Elsevier Sci Ltd, 2020) İnan, Berin; Göçmen, Rahşan; Çolpak, Ayşe İlksen; Meinl, Edgar; Karabudak, Rana; Tuncer, Aslı; Vural, Atay; Faculty Member; School of Medicine; 182369
    Background: To identify the clinical and radiological characteristics of adult patients with myelin oligodendrocyte glycoprotein antibody disease (MOG-AD) in a Turkish cohort. Methods: Clinical and radiological data were obtained retrospectively. Serological testing was done with fixed and live cell-based assays. Results: Optic neuritis was the most common presenting symptom, and neuromyelitis optica spectrum disorder (NMOSD) without aquaporin-4 antibody (AQP4-IgG) was the most common phenotype. Most patients had a relapsing course. Steroid dependency was common. Conus involvement was a frequent clinical and radiological feature. Radiological features such as long segment involvement and perineural optic nerve gadolinium enhancement were also typical in our cohort. One patient presented with encephalopathy and seizures, pointing out to the importance of testing of myelin oligodendrocyte antibody (MOG-IgG) in such patients as well. Conclusion: Myelin oligodendrocyte glycoprotein antibody disease is a heterogeneous clinical entity with characteristic clinical and radiological features. Our single-center experience underlines prominent clinical and magnetic resonance imaging (MRI) features and provides our treatment experiences.
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    Wireless sensor-based movement analysis is useful in detection of gait impairment within early stages of people with multiple sclerosis
    (Sage Publications Ltd, 2022) N/A; N/A; N/A; N/A; Akar, Kübra; Youssef, Hala; Altıntaş, Ayşe; Vural, Atay; Researcher; Researcher; Doktor; Doktor; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Koç University Hospital; Koç University Hospital; N/A; N/A; N/A; N/A
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    Myelin oligodendrocyte glycoprotein antibody associated central nervous system demyelinating disease: a tertiary center experience from Turkey (vol 44, 102376, 2020)
    (Elsevier Sci Ltd, 2021) İnan, Berin; Göçmen, RahŞan; Çolpak, Ayşe İlksen; Meinl, Edgar; Karabudak, Rana; Tuncer, Aslı; Vural, Atay; Faculty Member; School of Medicine; 182369
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    A novel homozygous FBXO38 variant causes an early-onset distal hereditary motor neuronopathy type IID
    (Nature Publishing Group (NPG), 2019) Akcimen, Fulya; Durmus, Hacer; Cakar, Arman; Houlden, Henry; Parman, Yesim G.; Vural, Atay; Başak, Ayşe Nazlı; Faculty Member; Faculty Member; School of Medicine; School of Medicine; 182369; 1512
    Distal hereditary motor neuronopathies (dHMN) are a genetically heterogeneous group of neuromuscular disorders caused by anterior horn cell degeneration and progressive distal muscle weakness. A heterozygous missense variant in FBXO38 has been previously described in two families affected by autosomal-dominant dHMN. In this paper, we describe a homozygous missense variant in FBXO38 (c.1577G>A; p.(Arg526Gln)) in a young Turkish female, offspring of consanguineous parents, with a congenital mild neuronopathy with idiopathic toe walking, normal sensory examination, and hearing loss. This work is the first to describe a novel homozygous variant and a suggested loss of function mechanism in FBXO38, expanding the dHMN type IID phenotype.