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PATIENT-DERIVED CSF FROM A CASE OF ANTI-DAGLA AUTOIMMUNE ENCEPHALITIS INDUCES SYNAPTIC DYSFUNCTION
Amelie Eichlerand 10 co-authors
Hannover Medical School
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-436
Presentation
Date TBA
Board: PS02-07PM-436
Event Information
Poster Board
PS02-07PM-436
Poster
View posterAbstract
Autoimmune encephalitis (AE) with antibodies against diacylglycerol-lipase-α (DAGLA) presents with cerebellar and limbic symptoms, but the cellular correlates of the disease remain unclear. We tested whether patient-derived CSF perturbs hippocampal neuronal networks, specifically focusing on excitatory synapses. Mouse organotypic entorhino-hippocampal tissue cultures were exposed to pathological CSF from one anti-DAGLA patient (p-CSF) or to non-pathological control CSF (c-CSF). We combined single-nucleus RNA-Seq, whole-cell patch-clamp recordings of dentate granule cells (dGCs) and CA1 pyramidal neurons (CA1-PNs), and post hoc morphometry of dendrites and synapses. We found significant alterations in dGCs, including excitatory synaptic transmission, membrane excitability, and action potential (AP) kinetics, while CA1-PNs remained mostly unaffected. Functional changes in dGCs were accompanied by layer-specific structural changes in dendritic morphologies and spines. Ultimately, we provide evidence that BTK-inhibition through tolebrutinib prevented synaptic dysfunction. These data define BTK-dependent excitatory synaptic changes in dGCs with glial involvement as a cellular correlate of anti-DAGLA-autoantibody mediated hippocampal pathology, employing organotypic tissue cultures as personalized functional screening tools.
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