The objective of the study was to determine the incidence of antibodies against neuronal surface antigens (NSA-ab) in patients with different types of epilepsy, in comparison with the subjects diagnosed with immune-mediated disorders. Forty patients with drug-resistant epilepsy (DRE) of unknown origin, 16 with post-stroke epilepsy, and 23 with systemic autoimmune disorders (SAD) with CNS involvement were included. NSA-ab were sought in serum using indirect immunofluorescence method. Relationships were analyzed between presence of NSA-ab and clinical presentation. NSA-ab was detected in the sera from five patients: anti-DPPX in one patient, anti-AMPAR1/R2 in two, anti-LGI1 in one and, in one case, both anti-CASPR2 and DPPX IgG. Out of these five patients, three represented the SAD subgroup and two the DRE subgroup. None of the patients with post-stroke epilepsy was positive for NSA-ab. Autoimmune etiology is worth considering in patients with drug-resistant epilepsy of unknown origin. The presence of NSA-ab in patients with systemic autoimmune disorders may be caused by unspecifically enhanced autoimmune reactivity. NSA-ab seem not to be related to epilepsy resulting from ischemic brain injury.
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http://dx.doi.org/10.3389/fneur.2021.660126 | DOI Listing |
J Vis Exp
January 2025
Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University;
Stroke is a leading cause of death and disability worldwide. Most cases of stroke are ischemic and result from the occlusion of the middle cerebral artery (MCA). Current pharmacological approaches for the treatment of ischemic stroke are limited; therefore, novel therapies providing effective neuroprotection against ischemic injury following stroke are urgently needed.
View Article and Find Full Text PDFTher Apher Dial
January 2025
Department of Neurology, Wakayama Medical University, Wakayama, Japan.
Introduction: Progressive encephalomyelitis with rigidity and myoclonus (PERM) is characterized by brainstem symptoms, muscle rigidity, and myoclonus. While autoantibodies to inhibitory neurons have been associated with the pathology, about 30% of cases are negative for autoantibodies. There are few reported cases of antibody-negative PERM and its clinical course and prognosis are unknown.
View Article and Find Full Text PDFMol Neurodegener
January 2025
Research Center for Neuroscience, Taipei Medical University, Taipei, Taiwan.
Chitinase-3-like-1 (CHI3L1) is an evolutionarily conserved protein involved in key biological processes, including tissue remodeling, angiogenesis, and neuroinflammation. It has emerged as a significant player in various neurodegenerative diseases and brain disorders. Elevated CHI3L1 levels have been observed in neurological conditions such as traumatic brain injury (TBI), Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), Creutzfeldt-Jakob disease (CJD), multiple sclerosis (MS), Neuromyelitis optica (NMO), HIV-associated dementia (HAD), Cerebral ischemic stroke (CIS), and brain tumors.
View Article and Find Full Text PDFJ Comp Neurol
January 2025
Institute of Neurobiology, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico.
Snails belonging to the genus Biomphalaria serve as obligatory intermediate hosts for the trematode Schistosoma mansoni, the causative agent for the most widespread form of schistosomiasis. The simpler nervous systems of gastropod molluscs, such as Biomphalaria, provide advantageous models for investigating neural responses to infection at the cellular and network levels. The present study examined neuropeptides related to cholecystokinin (CCK), a major multifunctional regulator of central nervous system (CNS) function in mammals.
View Article and Find Full Text PDFNeurol Neuroimmunol Neuroinflamm
March 2025
Institute for Clinical Neurobiology, University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Background And Objectives: Autoantibodies (aAbs) against glycine receptors (GlyRs) are mainly associated with the rare neurologic diseases stiff person syndrome (SPS) and progressive encephalomyelitis with rigidity and myoclonus (PERM). GlyR aAbs are also found in other neurologic diseases such as epilepsy. The aAbs bind to different GlyR α-subunits and, more rarely, also to the GlyR β-subunit.
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