Case report: Amnestic mild cognitive impairment in multiple domains associated with neurofascin 186 autoantibodies: Case series with follow-up and review

Niels Hansen; Anne Sagebiel; Kristin Rentzsch; Sina Hirschel; Jens Wiltfang; Björn H Schott; Bartels Claudia

doi:10.3389/fpsyt.2022.1054461

Case report: Amnestic mild cognitive impairment in multiple domains associated with neurofascin 186 autoantibodies: Case series with follow-up and review

Front Psychiatry. 2023 Jan 12:13:1054461. doi: 10.3389/fpsyt.2022.1054461. eCollection 2022.

Authors

Niels Hansen^{1

2}, Anne Sagebiel¹, Kristin Rentzsch³, Sina Hirschel¹, Jens Wiltfang^{1

4

5}, Björn H Schott^{1

4

6}, Bartels Claudia¹

Affiliations

¹ Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany.
² Department of Psychiatry and Psychotherapy, Translational Psychoneuroscience, University Medical Center Göttingen, Göttingen, Germany.
³ Clinical Immunological Laboratory Prof. Stöcker, Groß Grönau, Germany.
⁴ German Center for Neurodegenerative Diseases (DZNE), Göttingen, Germany.
⁵ Department of Medical Sciences, Neurosciences and Signaling Group, Institute of Biomedicine (iBiMED), University of Aveiro, Aveiro, Portugal.
⁶ Leibniz Institute for Neurobiology, University of Magdeburg, Magdeburg, Germany.

Abstract

Background: Neurofascin 186 autoantibodies are known to occur with a diseased peripheral nervous system. Recently, also additional central nervous system (CNS) involvement has been reported in conjunction with neurofascin 186 autoantibodies. Our case enlarges the spectrum of neurofascin 186 antibody-related disease to include mild cognitive impairment (MCI).

Methods: We report here a case after having examined the patient files retrospectively, including diagnostics such as blood and cerebrospinal fluid (CSF) analysis involving the determination of neural autoantibodies, brain magnetic resonance imaging (MRI), brain fluorodesoxyglucose positron emission tomography (FDG-PET), and extensive neuropsychological testing.

Results: We report on two patients with MCI. Brain MRI showed cerebral microangiopathy in both patients, but brain FDG-PET demonstrated pathology in the right prefrontal cortex, in the right inferior parietal cortex, and in both lateral occipital cortices in one patient. Neurofascin 186 antibodies were detected in serum in both patients, and neurofascin 186 autoantibodies were also detected in the CSF of one of these patients. At follow-up six month later, neurofascin 186 autoantibodies disappeared in one patient while persisting in the other.

Conclusion: We report on two individuals presenting MCI associated with neurofascin 186 antibodies, thus expanding the potential spectrum of neurofascin 186-associated disease. This report supports the recommendation to consider also neurofascin 186 autoantibodies in not just peripheral nerve disease, but also in disorders involving CNS autoimmunity. More studies are needed to clarify the lack of association between neurofascin 186 autoantibodies and cognitive decline.

Keywords: autoantibody; autoimmunity; cognition; mild cognitive impairment; neurofascin 186 antibody.

Publication types

Case Reports

Grants and funding

JW was supported by an Ilídio Pinho professorship, iBiMED (UIDB/04501/2020) at the University of Aveiro, Portugal. This study was funded by the Open Access fund of the University of Göttingen.