We investigated the effect of laquinimod on inflammatory demyelination, axonal damage, cytokine profiles and migratory capacities of lymphocytes in C57BL/6 mice with active EAE induced with MOG(35-55) peptide. The mice were treated at disease induction and after disease onset. Spinal cords were assessed histologically. Cytokines and adhesive properties were analyzed in splenocytes. Preventive and therapeutic laquinimod treatment reduced clinical signs, inflammation, and demyelination. VLA-4-mediated adhesiveness and pro-inflammatory cytokines such as IL-17 were down-regulated in treated animals. Within lesions, treated mice showed similar axonal densities, but less acute axonal damage than controls. Laquinimod might thus protect myelin and axons by decreasing pro-inflammatory cytokines and impairing the migratory capacity of lymphocytes.
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http://dx.doi.org/10.1016/j.jneuroim.2010.07.009 | DOI Listing |
Biomolecules
January 2025
Department of Neurology, Christian-Doppler University Hospital, Paracelsus Medical University, 5020 Salzburg, Austria.
Intrathecal immunoglobulin A (IgA) synthesis in multiple sclerosis (MS) has long earned little attention, despite a potential significance in disease pathogenesis and prognosis. The presence of IgA-positive plasma cells in MS lesions and along damaged axons suggests a role in disease pathogenesis. Available clinical evidence about a potential positive or negative prognostic role is scarce and inconclusive.
View Article and Find Full Text PDFInt J Pharm
January 2025
Université Paris-Saclay, Inserm, Maladies et hormones du système nerveux, 94276 Le Kremlin-Bicêtre, France. Electronic address:
Small interfering RNA (siRNA) has shown promising results for the treatment of Charcot-Marie-Tooth disease 1A (CMT1A) caused by overexpression of peripheral myelin protein (PMP22), leading to myelin dysfunction and axonal damage. Recently, we developed siRNA PMP22-squalene (SQ) nanoparticles (NPs) for intravenous use. Three consecutive injections of siRNA PMP22-SQ NPs at a cumulative dose of 1.
View Article and Find Full Text PDFJ Neurotrauma
January 2025
Regenerative Bioscience Center, University of Georgia, Athens, Georgia, USA.
Human neural stem cells (hNSCs) possess significant therapeutic potential for the treatment of traumatic brain injury (TBI), a leading cause of global death and disability. Recent pre-clinical studies have shown that hNSCs reduce tissue damage and promote functional recovery through neuroprotective and regenerative signaling and cell replacement. Yet the overall efficacy of hNSCs for TBI indications remains unclear.
View Article and Find Full Text PDFCells
January 2025
Department of Biochemistry, Hallym University College of Medicine, Chuncheon 24252, Kangwon-do, Republic of Korea.
Amyloid-β peptide (Aβ) is a critical cause of Alzheimer's disease (AD). It is generated from amyloid precursor protein (APP) through cleavages by β-secretase and γ-secretase. γ-Secretase, which includes presenilin, is regulated by several stimuli.
View Article and Find Full Text PDFBrain Sci
January 2025
CVJ Operative Unit, CVJ Research Center Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
: Diffusion tensor imaging (DTI), a variant of Diffusion Weighted Imaging (DWI), enables a neuroanatomical microscopic-like examination of the brain, which can detect brain damage using physical parameters. DTI's application to traumatic brain injury (TBI) has the potential to reveal radiological features that can assist in predicting the clinical outcomes of these patients. What is the ongoing role of DTI in detecting brain alterations and predicting neurological outcomes in patients with moderate to severe traumatic brain injury and/or diffuse axonal injury? : A scoping review of the PubMed, Scopus, EMBASE, and Cochrane databases was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines.
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