Journal of Neuroimmunology, Год журнала: 2024, Номер 393, С. 578384 - 578384
Опубликована: Июнь 4, 2024
Язык: Английский
Journal of Neuroimmunology, Год журнала: 2024, Номер 393, С. 578384 - 578384
Опубликована: Июнь 4, 2024
Язык: Английский
Journal of Neurology, Год журнала: 2025, Номер 272(2)
Опубликована: Янв. 15, 2025
Abstract Background BDNF has increasingly gained attention as a key molecule controlling remyelination with prominent role in neuroplasticity and neuroprotection. Still, it remains unclear how relates to clinicoradiological characteristics particularly at the early stage of disease where precise prognosis for further MS course is crucial. Methods BDNF, NfL GFAP concentrations serum CSF were assessed 106 treatment naïve patients (pwMS) well 73 other inflammatory/non-inflammatory neurological or somatoform disorders using single array HD-1 analyser. PwMS evaluated highly active profiles by applying aggressive criteria proposed ECTRIMS. Serum/CSF values logarithmically transformed compared across groups one-way ANOVA, while correlations calculated Pearson’s correlations. ROC analysis AUC comparisons diagnostic performance three biomarkers computed an explorative analysis. Results Serum (sBDNF) higher naïve pwMS onset after age 40 years ( p = 0.029), ≥2 gadolinium-enhancing lesions 0.009) motor, cerebellar, cognitive sphincter symptoms 0.036). correlated positively r 0.198, 0.014) 0.253, 0.002) serum, but not CSF. Neurological acute inflammatory relapse showed significantly sBDNF levels 0.03) controls, without did differ from controls 0.4). Better was found than sNfL sGFAP differentiating between vs. 2 more < 0.05) separating before years. Conclusion In pwMS, depending on disease-related characteristics, suggesting that only activity also capacities may vary severity. increased when neuroaxonal damage neurodegeneration, such GFAP, are elevated, possibly compensatory mechanism, reflect pathophysiological aspects beyond probably including apoptotic neuroinflammation.
Язык: Английский
Процитировано
2Frontiers in Neurology, Год журнала: 2024, Номер 15
Опубликована: Авг. 1, 2024
Neuroplasticity as a mechanism to overcome central nervous system injury resulting from different neurological diseases has gained increasing attention in recent years. However, deficiency of these repair mechanisms leads the accumulation neuronal damage and therefore long-term disability. To date, by which remyelination occurs why extent differs interindividually between multiple sclerosis patients regardless disease course are unclear. A member neurotrophins family, brain-derived neurotrophic factor (BDNF) received particular this context it is thought play role thus neuroplasticity, neuroprotection, memory.
Язык: Английский
Процитировано
8Journal of Neurology, Год журнала: 2024, Номер 271(6), С. 3512 - 3526
Опубликована: Март 27, 2024
Abstract Background Definitions of aggressive MS employ clinical and MR imaging criteria to identify highly active, rapidly progressing disease courses. However, the degree overlap between radiological parameters biochemical markers CNS injury is not fully understood. Aim this cross-sectional study was match hallmarks serum/CSF neuroaxonal astroglial (neurofilament light chain (sNfL, cNfL), glial fibrillary acidic protein (sGFAP, cGFAP)). Methods We recruited 77 patients with relapsing–remitting (RRMS) 22 clinically isolated syndrome. NfL GFAP levels in serum CSF were assessed using a single-molecule-array HD-1-analyzer. A general linear model each biomarker as dependent variable computed. Clinical MS, recently proposed by ECTRIMS Consensus Group, modeled independent variables. Other demographic, or laboratory parameters, covariates. Analyses repeated homogenous subgroup, consisting only newly diagnosed, treatment-naïve RRMS presenting an acute relapse. Results After adjusting for covariates multiplicity testing, sNfL cNfL concentrations strongly associated presence ≥2 gadolinium-enhancing lesions ( p = 0.00008; 0.004) well infratentorial on MRI 0.0003; < 0.004). No other correlated significantly CSF. In more homogeneous still 0.001), than 20 T2-lesions 0.049) 0.034), while 0.011) 0.029). Conclusions Among risk factors course, findings but characteristics marker should be given appropriate weight considering prognosis therapy. significant correlation detected alone.
Язык: Английский
Процитировано
5CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(12)
Опубликована: Дек. 1, 2024
Brain-derived neurotrophic factor (BDNF) is a neurotrophin, acting as signal and neuromodulator in the central nervous system (CNS). BDNF synthesized from its precursor proBDNF within CNS peripheral tissues. Through activation of NTRK2/TRKB (neurotrophic receptor tyrosine kinase 2), promotes neuronal survival, synaptic plasticity, growth, whereas it inhibits microglial release pro-inflammatory cytokines. dysregulated different neurodegenerative diseases depressions. However, there major controversy concerning levels stages multiple sclerosis (MS). Therefore, this review discusses potential role signaling MS, how modulators affect pathogenesis outcomes disease.
Язык: Английский
Процитировано
5Brain Sciences, Год журнала: 2024, Номер 14(3), С. 243 - 243
Опубликована: Фев. 29, 2024
Multiple sclerosis (MS) is a demyelinating central nervous system disease that leads to neurological disability. Brain-derived neurotrophic factors (BDNFs) are neurotrophins involved in neurodegenerative disorders. This study analysed the relationship between serum BDNF, disability and different MS treatments. We included 63 people with (PwMS), relapsing-remitting or clinically isolated syndrome, 16 healthy controls (HCs). levels of BDNF specific tests (Expanded Disability Status Scale, timed 25-foot walk test, nine-hole peg test), at baseline (V0) after one year interferon beta1a teriflunomide treatment (V1). Baseline values were not PwMS HCs (p = 0.85). The higher vs. 0.003). was related last-year relapses by duration (all p > 0.05). overall for decreased < 0.001). Both treatments implied similar reduction. influenced lesion burden, active lesions, new lesions on MRI In our cohort, had compared treatment. clinical paraclinical severity signs.
Язык: Английский
Процитировано
3Journal of Neuroimmunology, Год журнала: 2024, Номер 393, С. 578384 - 578384
Опубликована: Июнь 4, 2024
Язык: Английский
Процитировано
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