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Early Neuroaxonal Damage in Neurologic Disorders Associated With GAD65 Antibodies
Katharina Eisenhut1, Jennifer Faber1, Daniel Engels1
1From the Institute of Clinical Neuroimmunology (K.E.), University Hospital, Ludwig-Maximilians-Universität Munich; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität Munich, Martinsried; Graduate School of Sy; German Center for Neurodegenerative Diseases (DZNE) (J.F.); Department of Neurology, University Hospital Bonn, Germany; Institute of Clinical Neuroimmunology (D.E., R.G., T.K.), University Hospital, Ludwig-Maximilians-Universität Munich; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität Munich, Martinsried; Department of Neurology (J.L.), Ulm University; Department of Neurology (K.D., C.S.), University Hospital Würzburg; Institute of Clinical Chemistry (R.M.), University Hospital Schleswig-Holstein, Lübeck; Institute of Clinical Chemistry (K.K.F.), University Hospital Schleswig-Holstein, Kiel; Department of Neurology and Experimental Neurology (R.R., H.P.), Charité - Universitätsmedizin Berlin; German Center for Neurodegenerative Diseases (DZNE) Berlin; Department of Neurology and Experimental Neurology (C.F.), Charité - Universitätsmedizin Berlin; Section of Translational Neuroimmunology (J.W., C.G.), Department of Neurology, Jena University Hospital; Department of Neurology (D.R.), Hannover Medical School; Institute of Neuroimmunology and Multiple Sclerosis (L.K.P.), Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf; Department of Neurology (S.B., J.P.), University Medical Center of the Johannes Gutenberg University Mainz; Department of Neurology (A.K.), Martha-Maria Hospital Halle; Department of Neurology (J.K.), University Hospital Bochum; German Center for Neurodegenerative Diseases (DZNE) (B.N.), Munich; Metabolic Biochemistry, Faculty of Medicine, Biomedical Center (BMC), Ludwig-Maximilians-Universität München; and Institute of Clinical Neuroimmunology (F.S.T.), University Hospital, Ludwig-Maximilians-Universität Munich; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität Munich, Martinsried, Germany; Munich Cluster for Sys.
Objectives:
Neurodegeneration is considered a relevant pathophysiologic feature in neurologic disorders associated with antibodies against glutamic acid decarboxylase 65 (GAD65). In this study, we investigate surrogates of neuroaxonal damage in relation to disease duration and clinical presentation.
Methods:
In a multicentric cohort of 50 patients, we measured serum neurofilament light chain (sNfL) in relation to disease duration and disease phenotypes, applied automated MRI volumetry, and analyzed clinical characteristics.
Results:
In patients with neurologic disorders associated with GAD65 antibodies, we detected elevated sNfL levels early in the disease course. By contrast, this elevation of sNfL levels was less pronounced in patients with long-standing disease. Increased sNfL levels were observed in patients presenting with cerebellar ataxia and limbic encephalitis, but not in those with stiff person syndrome. Using MRI volumetry, we identified atrophy predominantly of the cerebellar cortex, cerebellar superior posterior lobe, and cerebral cortex with similar atrophy patterns throughout all clinical phenotypes.
Discussion:
Together, our data provide evidence for early neuroaxonal damage and support the need for timely therapeutic interventions in GAD65 antibody-associated neurologic disorders.
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