ArticleEMBO reports2024
Converging synaptic and network dysfunctions in distinct autoimmune encephalitis.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Anti-NMDAR encephalitis impairs intrinsic hippocampal dynamics through neuronal hypercoupling, hub dominance, and aberrant ensembles.Molecular psychiatry · 2026Article
- Multicolor Quantum Dot Tracking Uncovers Phenotypic Rescue of DAT A559V Aberrant Diffusion Upon D2R Antagonism.ACS chemical neuroscience · 2026Article
- Triple antibody-associated autoimmune encephalitis overlap: a case report of co-existing MOG-IgG, anti-NMDAR, and anti-mGluR5 positivity.Frontiers in immunology · 2026Article
- Glymphatic surrogate, choroid plexus remodeling, and exploratory brain network analysis in the post-acute phase of anti-NMDAR encephalitis: multimodal MRI evidence for cognitive associations and differential white matter mediation.Frontiers in immunology · 2026Article
- Longitudinal changes in [European journal of nuclear medicine and molecular imaging · 2026Article
- Diverse anti-NMDAR autoantibodies from individuals with encephalitis.Nature structural & molecular biology · 2024Article
- Human-derived monoclonal autoantibodies as interrogators of cellular proteotypes in the brain.Trends in neurosciences · 2024Review
- NMDA receptor autoantibodies primarily impair the extrasynaptic compartment.Brain : a journal of neurology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Psychiatric and neurological symptoms, as well as cognitive deficits, represent a prominent phenotype associated with variable forms of autoimmune encephalitis, regardless of the neurotransmitter receptor targeted by autoantibodies. The mechanistic underpinnings of these shared major neuropsychiatric symptoms remain however unclear. Here, we investigate the impacts of patient-derived monoclonal autoantibodies against the glutamatergic NMDAR (NMDAR mAb) and inhibitory GABAaR (GABAaR mAb) signalling in the hippocampal network. Unexpectedly, both excitatory and inhibitory synaptic receptor membrane dynamics, content and transmissions are altered by NMDAR or GABAaR mAb, irrespective of the affinity or antagonistic effect of the autoantibodies. The effect of NMDAR mAb on inhibitory synapses and GABAaR mAb on excitatory synapses requires neuronal activity and involves protein kinase signalling. At the cell level, both autoantibodies increase the excitation/inhibition balance of principal cell inputs. Furthermore, NMDAR or GABAaR mAb leads to hyperactivation of hippocampal networks through distinct alterations of principal cell and interneuron properties. Thus, autoantibodies targeting excitatory NMDAR or inhibitory GABAaR trigger convergent network dysfunctions through a combination of shared and distinct mechanisms.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.