2011
DOI: 10.1016/j.jns.2010.09.023
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NR2 antibodies: Risk assessment of transient ischemic attack (TIA)/stroke in patients with history of isolated and multiple cerebrovascular events

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Cited by 71 publications
(48 citation statements)
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“…The presence of IgG, IgM, and IgA subtypes of autoantibodies has been described [78]. Autoantibodies have also been reported in the serum of patients with stroke, including antineurofilament antibodies [79] and antibodies against the N-NR2A/2B subtype of the N-methyl-D-aspartate receptor (NMDAR) [80,81]. Nevertheless, the presence of some autoantibodies has been described in many different pathological conditions, and also in healthy subjects [82,83], but their clinical significance is not clear.…”
Section: Autoantibodiesmentioning
confidence: 99%
“…The presence of IgG, IgM, and IgA subtypes of autoantibodies has been described [78]. Autoantibodies have also been reported in the serum of patients with stroke, including antineurofilament antibodies [79] and antibodies against the N-NR2A/2B subtype of the N-methyl-D-aspartate receptor (NMDAR) [80,81]. Nevertheless, the presence of some autoantibodies has been described in many different pathological conditions, and also in healthy subjects [82,83], but their clinical significance is not clear.…”
Section: Autoantibodiesmentioning
confidence: 99%
“…However, patient 2 also had thrombosis of the femoral vein without previous catheter placement, suggesting that other factors may have contributed to thrombus formation. The specific mechanism underlying the association between anti-NMDAR encephalitis and venous thrombosis remains unknown, but might be partially related to the fact that autoantibodies to NMDAR are associated with a risk of other thrombotic diseases, including stroke, although the causal relationship remains unclear [9,10]. Nevertheless, because NMDAR is expressed in vascular endothelial cells and because its stimulation induces dilation of vessels [11], we speculate that vascular systems are damaged or functionally altered by autoantibodies to NMDAR.…”
Section: Discussionmentioning
confidence: 99%
“…Избыточная секре-ция глютамата, вызванная церебральной ишемией, приводит к гиперактивации рецепторов NMDA (N-метил-D-аспартат). Их избыточное количество (в особенности субъединицы NR2) отщепляется сери-новыми протеазами, проходит через ГЭБ, активиру-ет иммунную систему и вызывает образование анти-тел, а присутствие в крови свидетельствует о повы-шенном риске ТИА/инсульта (Weissman et al, 2011;Dambinova et al, 2012).…”
Section: результаты и обсуждениеunclassified