ArticleScientific reports2026
Pathogenic human autoantibodies against NMDA receptor alter dendritic spine size.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Antibody-Mediated Mechanisms in Autoimmune Neurological Disorders.The European journal of neuroscience · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis (NMDARE) is an autoimmune neurological disorder associated with anti-NMDAR antibodies (NMDAR-Ab), leading to synaptic dysfunction. While the effect of NMDAR-Ab on receptor internalization is well documented, its effect on dendritic protrusion morphology remains unclear. To investigate how NMDAR-Ab alters dendritic protrusion size and the associated molecular mechanisms using patient-derived sera. Cultured hippocampal neurons were treated with sera from patients with NMDARE. Protrusion size and the phosphorylation of cofilin, a regulator of actin dynamics, were also assessed. Exposure to NMDAR-Ab significantly decreased dendritic protrusion width and length while increasing protrusion density. Mechanistically, NMDAR-Ab decreased cofilin phosphorylation in dendritic protrusions. The reduction in spine size was partially reversible upon discontinuation of antibody treatment, except for the reduction in phosphorylated cofilin levels. NMDAR-Ab induced changes in dendritic protrusion size, along with alterations in actin dynamics, which may contribute to the cognitive and behavioral symptoms of NMDARE.
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