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Xenon is an inert gas with stable chemical properties which is used as an anesthetic. Recent in vitro and in vivo findings indicate that xenon also elicits an excellent neuroprotective effect in subanesthetic concentrations. The mechanisms underlying this primarily involve the attenuation of excitotoxicity and the inhibition of N-methyl-d-aspartic acid (NMDA) receptors and NMDA receptor-related effects, such as antioxidative effects, reduced activation of microglia, and Ca -dependent mechanisms, as well as the interaction with certain ion channels and glial cells. Based on this strong neuroprotective role, a large number of experimental and clinical studies have confirmed the significant therapeutic effect of xenon in the treatment of neurological diseases. This review summarizes the reported neuroprotective mechanisms of xenon and discusses its possible therapeutic application in the treatment of various neurological diseases.
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http://dx.doi.org/10.1002/jnr.24958 | DOI Listing |
J Neurol
September 2025
Department of Neurology, Xuanwu Hospital, National Center for Neurological Disorders, Capital Medical University, Beijing, China.
Background And Purpose: Efgartigimod has demonstrated efficacy in generalized myasthenia gravis (gMG) in both clinical trials and real-world studies. However, factors influencing early response have been less reported. This study aimed to evaluate the efficacy of efgartigimod in a multicenter gMG cohort and to identify the clinical factors associated with early therapeutic response.
View Article and Find Full Text PDFNat Cardiovasc Res
September 2025
Center for Vascular Research, Institute for Basic Science and Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
The meninges, consisting of the dura, arachnoid and pia mater that surround the brain and spinal cord, have been recognized from the earliest anatomical studies. First identified in 1787, lymphatic vessels in the dura are now receiving greater attention as their contribution to cerebrospinal fluid (CSF) clearance in diverse neurological conditions is being investigated. New methods have increased the understanding of dural lymphatics, but much is still being learned about their heterogeneity, intracranial and extracranial connections, and factors that govern their functions and maintenance.
View Article and Find Full Text PDFMol Psychiatry
September 2025
Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, NY, 14203, US.
Hyperphosphorylation of Tau and the ensuing microtubule destabilization are linked to synaptic dysfunction in Alzheimer's disease (AD). We find a marked increase of phosphorylated Tau (pTau) in cortical neurons differentiated from induced pluripotent stem cells (iPSCs) of AD patients. It is accompanied by significantly elevated expression of Serum and Glucocorticoid-regulated Kinase-1 (SGK1), which is induced by cellular stress, and Histone Deacetylase 6 (HDAC6), which deacetylates tubulin to destabilize microtubules.
View Article and Find Full Text PDFNat Genet
September 2025
Department of Neurology, School of Medicine, University of California, Davis, Sacramento, CA, USA.
To understand shared and ancestry-specific genetic control of brain protein expression and its ramifications for disease, we mapped protein quantitative trait loci (pQTLs) in 1,362 brain proteomes from African American, Hispanic/Latin American and non-Hispanic white donors. Among the pQTLs that multiancestry fine-mapping MESuSiE confidently assigned as putative causal pQTLs in a specific population, most were shared across the three studied populations and are referred to as multiancestry causal pQTLs. These multiancestry causal pQTLs were enriched for exonic and promoter regions.
View Article and Find Full Text PDFJ Neurol Neurosurg Psychiatry
September 2025
Department of Neurology, Rostock University Medical Center, Rostock, Germany.
Background: Multiple sclerosis (MS) is the most common neuroimmunological disease in young adults. Data on its clinical onset before the age of 18 (paediatric-onset MS (POMS)) are limited.
Methods: This observational study present data on >1000 POMS compared with adult-onset MS (AOMS) and analysed patients regarding diagnostic delay, initial symptoms and long-term outcome using generalised additive models and adjustment for relevant confounders.