Neurologic disorders associated with anti-glutamic acid decarboxylase antibodies: A comparison of anti-GAD antibody titers and time-dependent changes between neurologic disease and type I diabetes mellitus

Nakajima, Hideto; Nakamura, Yoshitsugu; Inaba, Yuiko; Tsutsumi, Chiharu; Unoda, Kiichi; Hosokawa, Takafumi; Kimura, Fumiharu; Hanafusa, Toshiaki; Date, Masamichi; Kitaoka, Haruko

doi:10.1016/j.jneuroim.2018.01.007

Cited by 28 publications

(27 citation statements)

References 40 publications

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“…Early diagnosis is, however, of utmost importance, since immunotherapy could be less effective, if not completely ineffective, when performed later over the course of the disease . In the diagnostic approach, it should be considered that neurologically asymptomatic patients with diabetes mellitus type 1 (DM1) can harbor GAD65‐Ab . The demonstration of an increased intrathecal synthesis (IS) of GAD65‐Ab is therefore particularly relevant in this setting to confirm that the neurologic syndrome is related to the GAD autoimmunity .…”

Section: Main Subtypes Of Ae and Pns Associated With Epilepsymentioning

confidence: 99%

“…IS can be calculated by using the following formula: [CSF GAD antibody titer/serum GAD antibody titer]/[CSF albumin/serum albumin] . Higher antibody titers, which tend to remain stable over time, characterize the immune‐mediated neurologic involvement and are important diagnostic clues that should orient the physician . It is notable that GAD antibody levels are not associated with the severity or the duration of the epilepsy, although a decline in the titer is commonly observed in patients who achieve a good seizure response after treatment .…”

Section: Main Subtypes Of Ae and Pns Associated With Epilepsymentioning

confidence: 99%

“…58,61 In the diagnostic approach, it should be considered that neurologically asymptomatic patients with diabetes mellitus type 1 (DM1) can harbor GAD65-Ab. 57,62 The demonstration of an increased intrathecal synthesis (IS) of GAD65-Ab is therefore particularly relevant in this setting to confirm that the neurologic syndrome is related to the GAD autoimmunity. 57,62 IS can be calculated by using the following formula: [CSF GAD antibody titer/serum GAD antibody titer]/[CSF albumin/serum albumin].…”

Section: Antibodies Against the Glutamate Decarboxylase 65 (Gad65) mentioning

confidence: 99%

“…57,62 The demonstration of an increased intrathecal synthesis (IS) of GAD65-Ab is therefore particularly relevant in this setting to confirm that the neurologic syndrome is related to the GAD autoimmunity. 57,62 IS can be calculated by using the following formula: [CSF GAD antibody titer/serum GAD antibody titer]/[CSF albumin/serum albumin]. 57 Higher antibody titers, which tend to remain stable over time, characterize the immune-mediated neurologic involvement and are important diagnostic clues that should orient the physician.…”

Section: Antibodies Against the Glutamate Decarboxylase 65 (Gad65) mentioning

confidence: 99%

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Seizure specificities in patients with antibody‐mediated autoimmune encephalitis

et al. 2019

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Accumulating data on patients with autoimmune encephalitis have shed light on specificities concerning clinical presentation and outcomes, which are dependent on the antigen targeted by the autoantibodies found in the patients’ cerebrospinal fluid or sera. Such specificities include seizure‐related clinical manifestations as well as the responsiveness to antiepileptic drugs. Although increased enthusiasm accompanies the discovery of novel antibodies and their associated clinical syndromes, several issues remain unsettled. First, it appears that therapy needs to be personalized in the view of the severity of each antibody‐mediated syndrome, patient‐related characteristics, and timing of treatment. Second, the lack of randomized controlled trials is a major drawback in the formulation of an appropriate immunotherapeutic strategy. In this review, we discuss the novel developments and challenges for the diagnosis and treatment of epilepsy in patients with well‐characterized autoimmune encephalitis, and delineate the principles for a rational approach toward precision medicine in this emerging field.

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Section: Main Subtypes Of Ae and Pns Associated With Epilepsymentioning

confidence: 99%

Section: Main Subtypes Of Ae and Pns Associated With Epilepsymentioning

confidence: 99%

Section: Antibodies Against the Glutamate Decarboxylase 65 (Gad65) mentioning

confidence: 99%

Section: Antibodies Against the Glutamate Decarboxylase 65 (Gad65) mentioning

confidence: 99%

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Seizure specificities in patients with antibody‐mediated autoimmune encephalitis

et al. 2019

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“…GAD (isoform GAD65) is a well-known target for autoantibodies in type I diabetes mellitus. Anti-GAD antibodies have also been described in several neurological diseases (mainly in epilepsy) but also in stiff-person syndrome, neuropathic pain, ataxia, and cerebellar disorders [16]. In a recent meta-analysis Grain et al [17] estimated the prevalence of GAD65 autoantibodies at 6.2% in BD, 5.8% in psychotic disorders, and 4.6% in schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Glutamate-Related Antibodies and Peripheral Insulin-Like Growth Factor in Bipolar Disorder and Lithium Prophylaxis

Ferensztajn‐Rochowiak

Kaczmarek

Wójcicka

et al. 2018

Neuropsychobiology

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Aims: The aim of this study was to evaluate serum levels of the antineuronal antibodies anti-N-methyl-D-aspartate receptor (NMDAR) and anti-glutamic acid decarboxylase (GAD), and insulin-like growth factor 1 (IGF-1), in patients with bipolar disorder (BD), during manic and depressive episodes and in remission compared to euthymic patients receiving long-term lithium therapy. Methods: Serum levels of anti-NMDAR and anti-GAD 450/620 antibodies, as well as IGF-1, were measured using the ELISA method in 19 manic and 17 depressed patients both in an acute episode and in remission after the episode. All of the subjects were under pharmacological treatment. The control group included 18 euthymic BD patients receiving lithium for 9–44 years (mean 22 ± 11) in whom a single measurement was performed. Results: Serum levels of anti-NMDAR antibodies were higher in acute manic episodes than in lithium-treated patients. Serum levels of anti-GAD 450/620 antibodies were higher in acute manic and depressive episodes compared to remission after the respective episode. Their values in both acute manic and depressive episodes were higher than those in lithium-treated patients. Serum levels of IGF-1 were higher in acute manic episodes and in remission after mania than in lithium-treated patients. Conclusion: Higher levels of anti-NMDAR and anti-GAD antibodies during episodes may point to an abnormality in the glutamatergic system in BD. Increased levels of IGF-1 during an acute manic episode and in remission after mania may constitute a compensatory mechanism against excitotoxicity. Lower levels of anti-NMDAR, anti-GAD antibodies, and IGF-1 during long-term lithium treatment may reflect normalization of this processes, contributing to mood stabilization.

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Serum glutamate decarboxylase antibodies and neurological disorders: when to suspect their association?

et al. 2021

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Neurologic disorders associated with anti-glutamic acid decarboxylase antibodies: A comparison of anti-GAD antibody titers and time-dependent changes between neurologic disease and type I diabetes mellitus

Cited by 28 publications

References 40 publications

Seizure specificities in patients with antibody‐mediated autoimmune encephalitis

Seizure specificities in patients with antibody‐mediated autoimmune encephalitis

Glutamate-Related Antibodies and Peripheral Insulin-Like Growth Factor in Bipolar Disorder and Lithium Prophylaxis

Serum glutamate decarboxylase antibodies and neurological disorders: when to suspect their association?

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