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Updated: Jan 19, 2026

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Neurochondrin neurological autoimmunity.

Shahar Shelly1, Thomas J Kryzer1, Lars Komorowski1

  • 1Department of Laboratory Medicine and Pathology (S.S., T.J.K., E.P.F., S.R.H., V.A.L., S.J.P., A.M.), Department of Neurology (E.P.F., V.A.L., S.J.P., A.M.), and Department of Immunology (V.A.L.), College of Medicine, Mayo Clinic; Euroimmun AG (L.K., R.M.), Lubeck, Germany; and Department of Neurology (M.D.A.), University of Mississippi Medical Center, Jackson, MS.

Neurology(R) Neuroimmunology & Neuroinflammation
|September 13, 2019
PubMed
Summary
This summary is machine-generated.

Neurochondrin autoimmunity typically causes rapidly progressive brainstem and cerebellar inflammation, often leading to poor outcomes. This condition may present with varied neurological symptoms and rarely be paraneoplastic.

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Area of Science:

  • Neurology
  • Immunology
  • Neuroscience

Background:

  • Neuroinflammation is a growing area of neurological research.
  • Autoimmune antibodies targeting neuronal proteins are increasingly identified as causes of neurological disorders.
  • Neurochondrin is a less-studied protein implicated in synaptic function.

Purpose of the Study:

  • To characterize the clinical spectrum and treatment responses in patients with neurochondrin-IgG positive encephalitis.
  • To identify the diagnostic features and outcomes associated with neurochondrin autoimmunity.

Main Methods:

  • Retrospective analysis of serum and cerebrospinal fluid (CSF) specimens screened for IgG antibodies.
  • Immunofluorescence assay on mouse hippocampal tissue to detect antibody binding patterns.
  • Recombinant protein assays to confirm antibody specificity for neurochondrin.

Main Results:

  • Eight patients were identified with neurochondrin-IgG antibodies, showing specific binding patterns in the CNS, particularly the hippocampus and cerebellum.
  • The majority of patients presented with rapidly progressive cerebellar ataxia and/or brainstem signs.
  • Immunotherapy in six patients with ataxia or brainstem signs resulted in poor functional outcomes, with only one remaining ambulatory; severe cerebellar atrophy was common on MRI.

Conclusions:

  • Neurochondrin autoimmunity is typically associated with rhombencephalitis, characterized by rapid progression and poor neurological outcomes.
  • While often nonparaneoplastic, other clinical phenotypes and rare paraneoplastic associations may occur.
  • This study highlights neurochondrin as a target in autoimmune neurological disorders.