Early Neuroaxonal Damage in Neurologic Disorders Associated With GAD65 Antibodies
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Early Neuroaxonal Damage in Neurologic Disorders Associated With GAD65 Antibodies. / Eisenhut, Katharina; Faber, Jennifer; Engels, Daniel; Gerhards, Ramona; Lewerenz, Jan; Doppler, Kathrin; Sommer, Claudia; Markewitz, Robert; Falk, Kim K; Rössling, Rosa; Pruess, Harald; Finke, Carsten; Wickel, Jonathan; Geis, Christian; Ratuszny, Dominica; Pfeffer, Lena K; Bittner, Stefan; Piepgras, Johannes; Kraft, Andrea; Klausewitz, Jaqueline; Nuscher, Brigitte; Kümpfel, Tania; Thaler, Franziska S; German Network for Research on Autoimmune Encephalitis (GENERATE).
In: NEUROL-NEUROIMMUNOL, Vol. 11, No. 1, 01.2024.Research output: SCORING: Contribution to journal › Short publication › Research › peer-review
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TY - JOUR
T1 - Early Neuroaxonal Damage in Neurologic Disorders Associated With GAD65 Antibodies
AU - Eisenhut, Katharina
AU - Faber, Jennifer
AU - Engels, Daniel
AU - Gerhards, Ramona
AU - Lewerenz, Jan
AU - Doppler, Kathrin
AU - Sommer, Claudia
AU - Markewitz, Robert
AU - Falk, Kim K
AU - Rössling, Rosa
AU - Pruess, Harald
AU - Finke, Carsten
AU - Wickel, Jonathan
AU - Geis, Christian
AU - Ratuszny, Dominica
AU - Pfeffer, Lena K
AU - Bittner, Stefan
AU - Piepgras, Johannes
AU - Kraft, Andrea
AU - Klausewitz, Jaqueline
AU - Nuscher, Brigitte
AU - Kümpfel, Tania
AU - Thaler, Franziska S
AU - German Network for Research on Autoimmune Encephalitis (GENERATE)
N1 - Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.
PY - 2024/1
Y1 - 2024/1
N2 - 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.
AB - 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.
KW - Humans
KW - Atrophy
KW - Autoantibodies
KW - Cerebellar Ataxia
KW - Nervous System Diseases
KW - Stiff-Person Syndrome
U2 - 10.1212/NXI.0000000000200176
DO - 10.1212/NXI.0000000000200176
M3 - Short publication
C2 - 37914416
VL - 11
JO - NEUROL-NEUROIMMUNOL
JF - NEUROL-NEUROIMMUNOL
SN - 2332-7812
IS - 1
ER -