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Related Experiment Video

Updated: Mar 6, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
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Microstructural visual system changes in AQP4-antibody-seropositive NMOSD.

Frederike C Oertel1, Joseph Kuchling1, Hanna Zimmermann1

  • 1NeuroCure Clinical Research Center (F.C.O., J.K., H.Z., C.C., F.S., J.B.-S., M.S., F.P., A.U.B.), and Department of Neurology (J.K., F.S., J.B.-S., K.R., F.P.), Charité-Universitätsmedizin Berlin; Department of Neurology (B.K., T.K.), Klinikum rechts der Isar, and Department of Experimental Neuroimmunology (T.K.), Technische Universität München; Munich Cluster for Systems Neurology (SyNergy) (T.K.), Germany; Clinical Ophthalmology and Eye Health (A.K.), Central Clinical School, Save Sight Institute, Sydney, Australia; and Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany.

Neurology(R) Neuroimmunology & Neuroinflammation
|March 4, 2017
PubMed
Summary
This summary is machine-generated.

Aquaporin-4 antibody-seropositive Neuromyelitis Optica Spectrum Disorders (NMOSD) patients without optic neuritis show early visual system changes. These microstructural alterations, particularly in the retina, suggest a primary astrocytopathy.

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Area of Science:

  • Neuroimmunology
  • Ophthalmology
  • Neuroimaging

Background:

  • Neuromyelitis Optica Spectrum Disorders (NMOSD) are autoimmune diseases targeting the central nervous system.
  • Aquaporin-4 antibodies (AQP4-ab) are key biomarkers for a subset of NMOSD patients.
  • Subtle visual pathway changes can occur even without overt clinical symptoms in NMOSD.

Purpose of the Study:

  • To detect early microstructural alterations in the afferent visual system of AQP4-ab-seropositive NMOSD patients.
  • To investigate these changes in patients lacking clinically apparent visual symptoms or lesions.
  • To differentiate between NMOSD patients with and without a history of optic neuritis (ON).

Main Methods:

  • Compared AQP4-ab-seropositive NMOSD patients with (NMOSD-ON) and without (NMOSD-LETM) prior ON, and healthy controls (HCs).
  • Utilized optical coherence tomography (OCT) to measure foveal thickness (FT), peripapillary retinal nerve fiber layer (pRNFL), and ganglion cell inner plexiform layer (GCIPL) thickness.
  • Employed diffusion tensor imaging (DTI) to assess microstructural integrity of the optic radiation (OR); visual acuity (VA) was also recorded.

Main Results:

  • Reduced FT was observed in both NMOSD-LETM and NMOSD-ON groups compared to HCs.
  • Fractional anisotropy reduction in the OR was detected in both NMOSD patient groups versus HCs.
  • Only NMOSD-ON patients exhibited neuroaxonal damage (pRNFL and GCIPL thinning); VA remained normal in NMOSD-LETM.

Conclusions:

  • AQP4-ab-seropositive NMOSD patients without a history of ON display subclinical microstructural changes in the afferent visual pathway.
  • The observed retinal changes, concentrated around the fovea, are indicative of a primary retinal astrocytopathy.
  • These findings highlight the potential for early detection of visual system involvement in NMOSD.