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The CD74 inhibitor DRhQ improves short-term memory and mitochondrial function in 5xFAD mouse model of Aβ accumulation.
Metab Brain Dis
January 2025
Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Neuroinflammation and mitochondrial dysfunction are early events in Alzheimer's disease (AD) and contribute to neurodegeneration and cognitive impairment. Evidence suggests that the inflammatory axis mediated by macrophage migration inhibitory factor (MIF) binding to its receptor, CD74, plays an important role in many central nervous system (CNS) disorders such as AD. Our group has developed DRhQ, a novel CD74 binding construct which competitively inhibits MIF binding, blocks macrophage activation and migration into the CNS, enhances anti-inflammatory microglia cell numbers and reduces pro-inflammatory gene expression.
View Article and Find Full Text PDFHyperreflective retinal foci are associated with retinal degeneration after optic neuritis in neuromyelitis optica spectrum disorders and multiple sclerosis.
Eur J Neurol
January 2025
Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine Berlin and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Background: Hyperreflective retinal foci (HRF) visualized by optical coherence tomography (OCT) potentially represent clusters of microglia. We compared HRF frequencies and their association with retinal neurodegeneration between people with clinically isolated syndrome (pwCIS), multiple sclerosis (pwMS), aquaporin 4-IgG positive neuromyelitis optica spectrum disorder (pwNMOSD), and healthy controls (HC)-as well as between eyes with (ONeyes) and without a history of optic neuritis (ONeyes).
Methods: Cross-sectional data of pwCIS, pwMS, and pwNMOSD with previous ON and HC were acquired at Charité-Universitätsmedizin Berlin.
Real-world multicentre cohort study on choices and effectiveness of immunotherapies in NMOSD and MOGAD.
J Neurol Neurosurg Psychiatry
December 2024
Department of Neurology and Institute of Neuroimmunology and MS (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Background: Recurrent attacks in neuromyelitis optica spectrum disorders (NMOSDs) or myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can lead to severe disability. We aimed to analyse the real-world use of immunotherapies in patients with NMOSD and MOGAD, focusing on changes in treatment strategies, effects on attack rates (ARR) and risk factors for attacks.
Methods: This longitudinal registry-based cohort study included 493 patients (320 with aquaporin-4 immunoglobulin G (AQP4-IgG) seropositive NMOSD (65%), 44 with AQP4-IgG seronegative NMOSD (9%) and 129 MOGAD (26%)) with 1247 treatments from 19 German and one Austrian centre from the registry of the neuromyelitis optica study group (NEMOS).
Longitudinal trajectories of digital upper limb biomarkers for multiple sclerosis.
Eur J Neurol
January 2025
Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
Background: Upper limb dysfunction is a common debilitating feature of relapsing-remitting multiple sclerosis (RRMS). We aimed to examine the longitudinal trajectory of the iPad®-based Manual Dexterity Test (MDT) and predictors of change over time.
Methods: We prospectively enrolled RRMS patients (limited to Expanded Disability Status Scale (EDSS) < 4).
Structures of Oligomeric States of Tau Protein, Amyloid-β, α-Synuclein and Prion Protein Implicated in Alzheimer's Disease, Parkinson's Disease and Prionopathies.
Int J Mol Sci
December 2024
Instituto de Histología y Embriología (IHEM), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), CC56, Universidad Nacional de Cuyo, Mendoza M5502JMA, Argentina.
In this review, we focus on the biophysical and structural aspects of the oligomeric states of physiologically intrinsically disordered proteins and peptides tau, amyloid-β and α-synuclein and partly disordered prion protein and their isolations from animal models and human brains. These protein states may be the most toxic agents in the pathogenesis of Alzheimer's and Parkinson's disease. It was shown that oligomers are important players in the aggregation cascade of these proteins.
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