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Journal articles on the topic 'Anti-GAD antibody'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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1

Seneviratne, Sinali O., Katherine A. Buzzard, Belinda Cruse, and Mastura Monif. "Cerebellar Ataxia Followed by Stiff Person Syndrome in a Patient with Anti-GAD Antibodies." Case Reports in Immunology 2020 (February 8, 2020): 1–4. http://dx.doi.org/10.1155/2020/8454532.

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Anti-GAD antibody syndrome is a result of the production of antibodies against glutamic acid decarboxylase (GAD), the main enzyme responsible for the production of gamma-aminobutyric acid (GABA). Several neurological manifestations including cerebellar ataxia and stiff person syndrome have been reported in association with anti-GAD antibodies. In this paper, we present a case of a young woman with anti-GAD antibodies who initially presented with cerebellar ataxia followed by stiff person syndrome three and a half years later. Having both cerebellar ataxia and stiff person syndrome is a rare oc

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Tsiortou, Popianna, Harry Alexopoulos, and Marinos C. Dalakas. "GAD antibody-spectrum disorders: progress in clinical phenotypes, immunopathogenesis and therapeutic interventions." Therapeutic Advances in Neurological Disorders 14 (January 2021): 175628642110034. http://dx.doi.org/10.1177/17562864211003486.

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Antibodies against glutamic acid decarboxylase (GAD), originally linked to stiff person syndrome (SPS), now denote the “ GAD antibody-spectrum disorders” ( GAD-SD) that also include autoimmune epilepsy, limbic encephalitis, cerebellar ataxia and nystagmus with overlapping symptomatology highlighting autoimmune neuronal excitability disorders. The reasons for the clinical heterogeneity among GAD-antibody associated syndromes remain still unsettled, implicating variable susceptibility of GABAergic neurons to anti-GAD or other still unidentified autoantibodies. Although anti-GAD antibody titers d

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Velardo, D., A. Nuara, V. Martinelli, G. Comi, and R. Fazio. "Anti-GAD antibody-positive myoclonic leg jerks." Neurological Sciences 36, no. 4 (2015): 647–48. http://dx.doi.org/10.1007/s10072-014-2058-0.

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4

Hao, R., and J. C. Schmit. "Cloning of the gene for glutamate decarboxylase and its expression during conidiation in Neurospora crassa." Biochemical Journal 293, no. 3 (1993): 735–38. http://dx.doi.org/10.1042/bj2930735.

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Neurospora crassa glutamate decarboxylase (GAD) is produced during conidiation and stored in dormant conidia. Polyclonal antibody was generated to GAD that had been purified to homogeneity. The anti-GAD antibody was specific for N. crassa GAD and inhibited GAD activity. The level of GAD protein decreased during conidial germination, indicating that GAD was degraded during this phase of development. The anti-GAD antibody was used to isolate a cDNA clone of GAD from a lambda ZAP cDNA expression library. Escherichia coli containing a plasmid with the cDNA insert produced GAD activity. The cDNA cl

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Journal, Baghdad Science. "Detection of Anti-Helicopacter pylori IgG Antibody, Anti-GAD antibody, Anti-Beta islets cell in a sample of serum with type-2 Diabetes mellitus patients." Baghdad Science Journal 10, no. 4 (2013): 1157–61. http://dx.doi.org/10.21123/bsj.10.4.1157-1161.

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We have investigated twenty five patients with type-2 diabetes mellitus aged (35-60) years and fifteen healthy persons as control group to detect Anti-Helicobacter pylori IgG antibody. All studied groups were carried out to measure fasting blood sugar, anti- Glutamic acid decarboxylase (GAD), anti-? islets cells antibody by IFAT, Anti-H. pylori IgG antibody by ELISA technique. There was significant elevation in the concentration of fasting blood sugar than in control group (P < 0.05), the patients had negative results for anti-GAD antibody and anti- ? islets cells antibody, there were signi

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Mezher, Izzat Abdul Satar, Noor Tha'ir Tahir Al-Khalidy, and Aufira Shaker Nsiaf. "Study of the prevalence of anti Glutamic Acid Decarboxylase antibody in Iraqi children and adolescent with type 1 Diabetes mellitus." Al Mustansiriyah Journal of Pharmaceutical Sciences 10, no. 2 (2011): 114–22. http://dx.doi.org/10.32947/ajps.v10i2.301.

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Type 1 diabetes mellitus is a disease caused by the progressive and selective destruction, by autoimmune mechanisms, of pancreatic beta cells.Recent findings support this autoimmune character, and various autoimmune markers have been described in type1 diabetes, a number of specific and nonspecificantigens have been identified. The major autoantigen involved in the destructive process of beta-cells leading to the development of type 1 diabetes is glutamic acid decarboxylase (GAD).The aim of the present study was to assess the occurrence of anti-glutamic acid decarboxylase (Anti-GAD) antibodies

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Awad, Amer, Olaf Stüve, Marlyn Mayo, Rafeed Alkawadri, and Bachir Estephan. "Anti-Glutamic Acid Decarboxylase Antibody-Associated Ataxia as an Extrahepatic Autoimmune Manifestation of Hepatitis C Infection: A Case Report." Case Reports in Neurological Medicine 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/975152.

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Extrahepatic immunological manifestations of hepatitis C virus (HCV) are well described. In addition, antiglutamic acid decarboxylase (GAD) antibody-associated cerebellar ataxia is well-established entity. However, there have been no reports in the literature of anti-GAD antibody-associated ataxia as an extrahepatic manifestation of HCV infection. We report the case of a young woman with chronic hepatitis C virus and multiple extrahepatic autoimmune diseases including Sjögren syndrome and pernicious anemia who presented with subacute midline cerebellar syndrome and was found to have positive a

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8

Brown, Rachel, Gilbert Thomas-Black, Hector Garcia-Moreno, et al. "Clinical relevance and utility of GAD65 antibodies in neurological disease: an eight year cohort study." Journal of Neurology, Neurosurgery & Psychiatry 93, no. 9 (2022): e2.173. http://dx.doi.org/10.1136/jnnp-2022-abn2.28.

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Neurological syndromes associated with glutamic acid decarboxylase (GAD) antibodies provide a challenge in understanding disease pathogenesis, interpreting antibody results, and deciding manage- ment. We retrospectively reviewed 277 patients with positive anti-GAD antibodies (≥ 10 IU/mL) at our centre between 2012-2020. 154 (56%) had one or more neurological disorders including 27 stiff person spectrum disorders (SPSD) (18%), 20 cerebellar ataxia (13%), 18 epilepsy (12%), 18 encephalitis (12%),12 ‘mixed’ (8%), and 59 other neurological disorders (38%). Co-existing autoimmunity was common; 57 (

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9

Gillinder, Lisa, Tamara Powell, Donald Craig, Stephen Walsh, David Gillis, and Pamela McCombe. "HLA typing in anti-GAD antibody associated epilepsy." Epilepsy & Behavior 163 (February 2025): 110179. https://doi.org/10.1016/j.yebeh.2024.110179.

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10

Nanri, Kazunori, Hisayoshi Niwa, Hiroshi Mitoma, et al. "Low-Titer Anti-GAD-Antibody-Positive Cerebellar Ataxia." Cerebellum 12, no. 2 (2012): 171–75. http://dx.doi.org/10.1007/s12311-012-0411-5.

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Shargian-Alon, Liat, Pia Raanani, Uri Rozovski, Tali Siegal, Shlomit Yust-Katz, and Moshe Yeshurun. "Immune Mediated Cerebellar Ataxia: An Unknown Manifestation of Graft-versus-Host Disease." Acta Haematologica 141, no. 1 (2018): 19–22. http://dx.doi.org/10.1159/000494423.

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Neurologic complications of allogeneic hematopoietic cell transplantation (allo-HCT) include infections, cerebrovascular events, therapy-induced neurotoxicity, recurrent malignancies, and neurologic manifestations of graft-versus-host disease (GVHD). Anti-glutamic acid decarboxylase (GAD) antibody-associated cerebellar ataxia is a well-established disorder of autoimmune origin, but there are no reports in the literature of its occurrence following allo-HCT. We describe a middle-aged woman with chronic GVHD after allo-HCT who presented with a rapidly progressive cerebellar syndrome. Thorough in

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Tran, Thua Nguyen. "Evaluation the relation between age at the time of diabetes diagnosis and Glutamic acid decarboxylase (GAD) antibody in non- overweight, obese diabetic individuals." Vietnam Journal of Diabetes and Endocrinology, no. 40 (January 28, 2021): 39–44. http://dx.doi.org/10.47122/vjde.2020.40.7.

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Objective: Evaluation the relation between age at the time of diabetes diagnosis and glutamic acid decarboxylase (GAD) antibody in non- overweight, obese diabetic individuals. Method: A cross-sectional study on 284 non overweight- obesity diabetic patients at Hue Central hospital from August 2017 to August 2019. All patients were measured autoantibodies glutamic acid decarboxylase (anti-GAD). GAD antibody- positive was determined when autoantibodies to GAD concentration was higher than 5 IU/mL. Clinical data (age, sex, weight, hight) were obtained. Age at the time of diabetes diagnosis was int

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Dal, Shoaib, and Bill O’Brien. "076 A rare case of anti-glutamate decarboxylase antibody syndrome presenting with recurrent vomiting." Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (2019): A24.1—A24. http://dx.doi.org/10.1136/jnnp-2019-anzan.64.

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IntroductionAnti-glutamte decarboxylase antibody (anti-GAD) has been linked with various neurological syndromes including stiff-person syndrome, limbic encephalopathy, cerebellar ataxia, eye movement disorders and epilepsy (collectively known as ‘anti-GAD positive neurological syndromes’).1 We describe a very atypical phenotypic presentation of anti-GAD syndrome with unexplained vomiting and weight loss.CaseA 46 years old lady with no past medical or family history of note, presented with 6 months history of severe headaches and recurrent attacks of episodic vomiting (4–6 episodes of multiple

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Manzke, Pedro, Talyta Grippe, Georgia L. Tavares, et al. "Anti-GAD Antibody-associated Syndrome Presenting with Limb Myoclonus." Tremor and Other Hyperkinetic Movements 8 (November 1, 2018): 590. http://dx.doi.org/10.5334/tohm.421.

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15

Kanter, Ines C., Hagen B. Huttner, Dimitre Staykov, et al. "Cyclophosphamide for anti-GAD antibody-positive refractory status epilepticus." Epilepsia 49, no. 5 (2008): 914–20. http://dx.doi.org/10.1111/j.1528-1167.2007.01500.x.

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16

Chang, Chiung-Chih, Scott D. Eggers, Julene K. Johnson, Aissa Haman, Bruce L. Miller, and Michael D. Geschwind. "Anti-GAD antibody cerebellar ataxia mimicking Creutzfeldt–Jakob disease." Clinical Neurology and Neurosurgery 109, no. 1 (2007): 54–57. http://dx.doi.org/10.1016/j.clineuro.2006.01.009.

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17

Zhou, Feng C., Christine Cheng, and Sharon Bledsoe. "Establishment of a Stable Glutamate Decarboxylase (Gad) Expressing Cell-Line by Transfection." Cell Transplantation 2, no. 3 (1993): 193–205. http://dx.doi.org/10.1177/096368979300200303.

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We have constructed a recombinant DNA clone containing the gene encoding glutamic acid decarboxylase (GAD), which catalyzes the synthesis of γ-amino-butyric acid (GABA). This recombinant DNA was then transfected into mouse NIH-3T3 fibroblast cells for transplantation into Swiss-Web mice. In order to construct a plasmid capable of transcribing the DNA insert in the eucaryotic cells, the GAD gene was removed from pSP65-13, and was ligated into the vector pSV2neo, which contains the SV40 early promoter, and the neomycin resistance gene. The pSV2GAD was then transfected into NIH-3T3 fibroblasts by

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18

Zhang, Chen, Yuwei Dai, Binhong Han, et al. "A Case of Anti-GAD 65 Autoimmune Encephalitis Associated with Focal Segmental Stiff-Person Syndrome." Brain Sciences 13, no. 2 (2023): 369. http://dx.doi.org/10.3390/brainsci13020369.

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Glutamic acid decarboxylase (GAD) antibody-related encephalitis is an autoimmune disease associated with intracellular neuronal antigens. We report on a rare case of GAD antibody-associated encephalitis complicated with focal segmental stiffness-person syndrome (SPS) in a middle-aged woman. The disease course lasted for >10 years, initially presenting with drug-resistant epilepsy, followed by stiffness of the right lower limb, and right upper limb involvement. The patient experienced anxiety and depression symptoms due to long-term illness. During hospitalization, serum and cerebrospinal fl

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19

Sköldberg, Filip, Fredrik Rorsman, Jaakko Perheentupa, et al. "Analysis of Antibody Reactivity against Cysteine Sulfinic Acid Decarboxylase, A Pyridoxal Phosphate-Dependent Enzyme, in Endocrine Autoimmune Disease." Journal of Clinical Endocrinology & Metabolism 89, no. 4 (2004): 1636–40. http://dx.doi.org/10.1210/jc.2003-031161.

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Abstract The structurally related group II pyridoxal phosphate (PLP)-dependent amino acid decarboxylases glutamic acid decarboxylase (GAD), aromatic l-amino acid decarboxylase (AADC), and histidine decarboxylase (HDC) are known autoantigens in endocrine disorders. We report, for the first time, the prevalence of serum autoantibody reactivity against cysteine sulfinic acid decarboxylase (CSAD), an enzyme that shares 50% amino acid identity with the 65- and 67-kDa isoforms of GAD (GAD-65 and GAD-67), in endocrine autoimmune disease. Three of 83 patients (3.6%) with autoimmune polyendocrine syndr

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20

Ozmen, Sevgi, Esra Demirci, Didem Behice Oztop, Fatih Kardas, Selma Gokahmetoglu, and Huseyin Per. "Anti-Ganglioside, Anti-Glutamate, and Anti-Gad Antibody Levels in Attention-Deficit Hyperactivity Disorder." Erciyes Tıp Dergisi/Erciyes Medical Journal 37, no. 2 (2015): 48–50. http://dx.doi.org/10.5152/etd.2015.9356.

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21

Stayoussef, Mouna, Jihen Benmansour, Fayza A. Al-Jenaidi, et al. "Glutamic Acid Decarboxylase 65 and Islet Cell Antigen 512/IA-2 Autoantibodies in Relation to Human Leukocyte Antigen Class II DR and DQ Alleles and Haplotypes in Type 1 Diabetes Mellitus." Clinical and Vaccine Immunology 18, no. 6 (2011): 990–93. http://dx.doi.org/10.1128/cvi.00073-11.

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ABSTRACTThe frequencies of autoantibodies against glutamic acid decarboxylase 65 (GAD65) and islet cell antigen (ICA) 512/IA-2 (512/IA-2) are functions of the specific human leukocyte antigen (HLA) in type 1 diabetes mellitus (T1D). We investigated the association of HLA class II (DR and DQ) alleles and haplotypes with the presence of GAD and IA-2 autoantibodies in T1D. Autoantibodies were tested in 88 Tunisian T1D patients and 112 age- and gender-matched normoglycemic control subjects by enzyme immunoassay. Among T1D patients, mean anti-GAD antibody titers were higher in theDRB1*030101allele

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22

Shivaram, Sumanth, Ashok V. Reddy Tallapalli, Manisha Gupta, Saraswati Nashi, Girish B. Kulkarni, and Suvarna Alladi. "Spontaneous Downbeat Nystagmus in Anti-GAD-Antibody-Associated Paraneoplastic Syndrome." Journal of Neurosciences in Rural Practice 13, no. 03 (2022): 546–49. http://dx.doi.org/10.1055/s-0042-1749404.

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AbstractSpontaneous downbeat nystagmus and ocular flutter are rare clinical signs. Such findings are commonly related to cerebellar pathology, predominantly ischemia. In a significant percentage of patients, the cause may not be found. If these signs are associated with ataxia, cognitive decline, and seizure, anti-glutamic acid decarboxylase-associated neurological syndrome must be suspected. Background history of tumor has to be enquired. Treatment with immune modulation helps in partial recovery of such cases.

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Schiff, David, Josep Dalmau, and Delynne J. Myers. "Anti-GAD Antibody Positive Stiff-Limb Syndrome in Multiple Myeloma." Journal of Neuro-Oncology 65, no. 2 (2003): 173–75. http://dx.doi.org/10.1023/b:neon.0000003754.34527.f2.

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Nagai, Koki, Takanobu Maekawa, Hiroshi Terashima, Masaya Kubota, and Akira Ishiguro. "Severe anti-GAD antibody-associated encephalitis after stem cell transplantation." Brain and Development 41, no. 3 (2019): 301–4. http://dx.doi.org/10.1016/j.braindev.2018.10.006.

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SATO, Seijiro, and Masanori TSUCHIDA. "A Case of Thymoma with Anti-GAD Antibody Positive Myasthenia Gravis." Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) 74, no. 8 (2013): 2101–5. http://dx.doi.org/10.3919/jjsa.74.2101.

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Hong, Eun-Gyoung. "Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea." Korean Diabetes Journal 33, no. 1 (2009): 13. http://dx.doi.org/10.4093/kdj.2009.33.1.13.

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Lee, Sang Ah, Eui Young Kim, Eun Hee Kim, et al. "Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea." Korean Diabetes Journal 33, no. 1 (2009): 16. http://dx.doi.org/10.4093/kdj.2009.33.1.16.

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Eggenberger, Eric R., Andrew G. Lee, Madhavi Thomas, and Eugene C. Lai. "Neuro-Ophthalmologic Findings in Patients with the Anti-GAD Antibody Syndrome." Neuro-Ophthalmology 30, no. 1 (2006): 1–6. http://dx.doi.org/10.1080/01658100600599410.

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Wang, F., G. Wilmot, and A. G. Shaikh. "Determinants of motor restoration in the syndrome of anti-GAD antibody." Journal of the Neurological Sciences 405 (October 2019): 367. http://dx.doi.org/10.1016/j.jns.2019.10.1534.

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Flores-Cantu, Hazael, Carlos R. Camara-Lemarroy, Hector J. Calderon-Hernandez, Maria A. Zapata-Rivera, Jesus Z. Villareal-Perez, and Hector J. Villareal-Velazquez. "Anti-GAD Antibody, Seizures, Cerebellar Ataxias and Vitiligo: A Diagnostic Challenge." Cerebellum 14, no. 3 (2015): 375–77. http://dx.doi.org/10.1007/s12311-014-0625-9.

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Kern, Kristina, and Brooke A. Shuster. "Rare presentation of anti-GAD-65 antibody-positive autoimmune encephalitis and simultaneous onset of type 1 diabetes mellitus in a paediatric patient." BMJ Case Reports 14, no. 3 (2021): e237913. http://dx.doi.org/10.1136/bcr-2020-237913.

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A 16-year-old female patient presented with subacute onset of headaches, changes in acute mental status, expressive aphasia and auditory hallucinations. New oedema and enhancement of the temporal lobe were seen on brain MRI, with correlating subclinical seizures seen on electroencephalogram. Simultaneously, our patient was diagnosed with new-onset type 1 diabetes mellitus, with positive anti-glutamic acid decarboxylase (anti-GAD-65) antibodies in the serum. Cerebrospinal fluid studies remained negative, including anti-GAD-65 antibodies. Clinical remission was achieved with corticosteroids and

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Çoban, Arzu, Cem İsmail Küçükali, Başar Bilgiç, et al. "Evaluation of Incidence and Clinical Features of Antibody-Associated Autoimmune Encephalitis Mimicking Dementia." Behavioural Neurology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/935379.

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Background. Anti-neuronal autoimmunity may cause cognitive impairment that meets the criteria for dementia.Objective. Our aim was to detect the incidence and clinical features of autoimmune encephalitis imitating clinical findings of primary dementia disorders and to delineate the validity of anti-neuronal antibody screening in dementia patients.Methods. Fifty consecutive patients fulfilling the clinical criteria for primary dementia, 130 control patients, and 50 healthy controls were included. Their sera were investigated for several ion channel and glutamic acid decarboxylase (GAD) antibodie

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Aguiar, Tiago Silva, Andrea Fragoso, Carolina Rouanet de Albuquerque, et al. "Clinical characteristics of patients with cerebellar ataxia associated with anti-GAD antibodies." Arquivos de Neuro-Psiquiatria 75, no. 3 (2017): 142–46. http://dx.doi.org/10.1590/0004-282x20170011.

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ABSTRACT The enzyme glutamic acid decarboxylase (GAD), present in GABAergic neurons and in pancreatic beta cells, catalyzes the conversion of gamma-aminobutyric acid (GABA). The cerebellum is highly susceptible to immune-mediated mechanisms, with the potentially treatable autoimmune cerebellar ataxia associated with the GAD antibody (CA-GAD-ab) being a rare, albeit increasingly detected condition. Few cases of CA-GAD-ab have been described. Methods This retrospective and descriptive study evaluated the clinical characteristics and outcomes of patients with CA-GAD-ab. Result Three patients with

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Gilerovitch, Helen G., Georgia A. Bishop, James S. King, and Richard W. Burry. "Demonstration of GAD in purkinje-cell terminals with silver enhanced gold immunocytochemistry." Proceedings, annual meeting, Electron Microscopy Society of America 51 (August 1, 1993): 288–89. http://dx.doi.org/10.1017/s0424820100147284.

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The neurotransmitter gamma-amino butyric acid (GABA) is synthesized in presynaptic terminals by glutamic acid decarboxylase (GAD). Antibodies to GAD have been used to localize presynaptic terminals in the cerebellar cortex that use GABA as a neurotransmitter. In the cerebellum, the Purkinje cell makes synaptic contacts on dendrites and somata of neurons in the cerebellar nuclei. We were interested in developing a technique that combined light microscopic analysis of GAD distribution in Purkinje cell terminals with high quality electron microscopic localization of GAD.The approach taken in this

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Ates, I., M. F. Arikan, K. Erdogan, et al. "Factors associated with increased irisin levels in the type 1 diabetes mellitus." Endocrine Regulations 51, no. 1 (2017): 1–7. http://dx.doi.org/10.1515/enr-2017-0001.

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Abstract Objective. The aim of the present study was to determine the irisin levels in patients with the type 1 diabetes mellitus (T1DM) and to examine the relation of irisin levels with the inflammation and autoimmunity.Methods. This study included 35 cases diagnosed with T1DM and 36 healthy volunteers. Antiglutamic acid decarboxylase (anti-GAD), islet cell antibody (ICA), and insulin autoantibody levels were measured in patients at the time when they were included into the study and recorded from the patient files. Serum irisin levels were measured by ELISA kit.Results. The median irisin lev

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AKMAN, CIGDEM I., MARC C. PATTERSON, ARYE RUBINSTEIN, and RONIT HERZOG. "Limbic encephalitis associated with anti-GAD antibody and common variable immune deficiency." Developmental Medicine & Child Neurology 51, no. 7 (2009): 563–67. http://dx.doi.org/10.1111/j.1469-8749.2008.03217.x.

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Triplett, J., S. Vijayan, A. MacDonald, et al. "Fulminant Anti-GAD antibody encephalitis presenting with status epilepticus requiring aggressive immunosuppression." Journal of Neuroimmunology 323 (October 2018): 119–24. http://dx.doi.org/10.1016/j.jneuroim.2018.06.013.

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Baroncini, D., F. Spagnolo, L. Sarro, G. Comi, and M. A. Volonte’. "A complex case of anti-GAD antibody-related syndrome treated with Rituximab." Neurological Sciences 34, no. 10 (2013): 1847–49. http://dx.doi.org/10.1007/s10072-013-1327-7.

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Jeong, Ji Hoon, Minhyung Lee, Won Jong Kim, et al. "Anti-GAD antibody targeted non-viral gene delivery to islet beta cells." Journal of Controlled Release 107, no. 3 (2005): 562–70. http://dx.doi.org/10.1016/j.jconrel.2005.07.010.

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Apparow, Saraswathy, and Cheah Cheng Foong. "CEREBELLAR ATAXIA ASSOCIATED WITH ANTI-GLUTAMIC ACID DECARBOXYLASE ANTIBODIES: A CASE REPORT." Journal of the ASEAN Federation of Endocrine Societies 37 (July 15, 2022): 42. https://doi.org/10.15605/jafes.037.s2.42.

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INTRODUCTIONAnti-glutamic acid decarboxylase (anti-GAD) - related cerebellar ataxia is the second most common cause of GAD antibody (Ab) spectrum disorders. It is characterised by cerebellar symptoms with elevated GAD Ab levels in the serum and cerebrospinal fluid (CSF). It commonly affects females associated with Type 1 DM or polyendocrinopathy. IVIG is the most effective immunomodulatory therapy. CASEWe report a 34-year-old male diagnosed with Type1 DM with high titer of serum anti-GAD Ab who first presented with cerebellar syndrome at the age of 12. At 15 years of age, Hba1c was 12% hence,

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Balakhadze, Mariam, Elene Giorgadze та Marina Lomidze. "The Frequency of Langerhans Isletsβ-Cells Autoantibodies (Anti-GAD) in Georgian Children and Adolescents with Chronic Autoimmune Thyroiditis". International Journal of Endocrinology 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/6597091.

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Aim. Chronic autoimmune thyroiditis and type 1 diabetes mellitus are organ-specific autoimmune diseases. There is large evidence that autoimmunity against the thyroid gland in patients with type 1 diabetes mellitus is increased, but little is known about anti-islet cell autoimmune status in patients with chronic autoimmune thyroiditis. We evaluated the concentration of antibodies against glutamic acid decarboxylase (GAD) which are widely used as a diagnostic and predictive tool for type 1 diabetes mellitus, in school-aged Georgian children with chronic autoimmune thyroiditis.Methods. The frequ

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MASUDA, Katsuhiko, Kazuhiko YAMAMOTO, and Norihiko AOKI. "Measurement of Anti-Glutamate Decarboxylase (GAD) Antibody by Dot-Blot Assay Using Purified Rat Brain GAD Preparation and Synthetic Peptides of GAD-Basic Study." Folia Endocrinologica Japonica 72, no. 4 (1996): 687–707. http://dx.doi.org/10.1507/endocrine1927.72.4_687.

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Moreira, Marina Carolina, Gustavo Müller Lara, Rafael Linden, et al. "Frequency of the anti-glutamic acid decarboxylase immunological marker in patients with diabetes duration longer than three years in southern Brazil." Sao Paulo Medical Journal 129, no. 3 (2011): 130–33. http://dx.doi.org/10.1590/s1516-31802011000300002.

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CONTEXT AND OBJECTIVE: The anti-GAD (glutamic acid decarboxylase) antibody is considered to be an important marker for type 1 diabetes mellitus (DM1), with frequency that varies depending on the population studied and the duration of the disease. Therefore, the aim of this study was to determine the frequency of this autoantibody in a group of patients in southern Brazil with DM1 that had been diagnosed more than three years previously. DESIGN AND SETTING: Analytical cross-sectional study with a control group conducted at the Biomedicine Laboratory of Universidade Feevale. METHODS: This study

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Nuzhnyi, E. P., M. Yu Krasnov, D. R. Akhmadullina, A. A. Abramova, E. Yu Fedotova, and S. N. Illarioshkin. "Ataxia associated with anti-glutamic acid decarboxylase antibodies." Neurology, Neuropsychiatry, Psychosomatics 12, no. 5 (2020): 66–70. http://dx.doi.org/10.14412/2074-2711-2020-5-66-70.

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Anti-glutamic acid decarboxylase (GAD) antibody-associated ataxia is a rarely diagnosed but potentially curable disease associated with autoimmune damage to and death of Purkinje cells in the cerebellar cortex. In Russia, the authors have provided for the first time descriptions of three own observations of this disease, which had a number of clinical features, such as slow progression, mild ataxia, stroke-like episodes with stem symptoms, concomitant gluten sensitivity, onset of ataxia after hepatitis C with cerebellar hemiataxia and hemiatrophy. In the all patients, the diagnosis was verifie

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Dalakas, M. C., M. Fujii, M. Li, and B. McElroy. "The clinical spectrum of anti-GAD antibody-positive patients with stiff-person syndrome." Neurology 55, no. 10 (2000): 1531–35. http://dx.doi.org/10.1212/wnl.55.10.1531.

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Dubbioso, Raffaele, Vincenzo Marcelli, Fiore Manganelli, Rosa Iodice, Marcello Esposito, and Lucio Santoro. "Anti-GAD antibody ocular flutter: expanding the spectrum of autoimmune ocular motor disorders." Journal of Neurology 260, no. 10 (2013): 2675–77. http://dx.doi.org/10.1007/s00415-013-7110-0.

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Valinčiūtė, Justina, Neringa Jucevičiūtė, Renata Balnytė, Giedrė Jurkevičienė, and Giedrė Gelžinienė. "GAD65 Antibody-Associated Epilepsy." Medicina 59, no. 6 (2023): 1135. http://dx.doi.org/10.3390/medicina59061135.

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Autoimmune processes are an increasingly recognized cause of seizures. Antibodies against neuronal surface antigens are implicated in the development of acute symptomatic seizures secondary to autoimmune encephalitis, whereas antibodies against intracellular antigens (anti-glutamic acid decarboxylase (GAD) and onconeural antibodies) are found in cases of autoimmune-associated epilepsy (AAE). AAE is described as isolated drug-resistant epilepsy without any specific magnetic resonance imaging (MRI) or cerebrospinal fluid changes and with a very limited response to immunotherapy. We present a cli

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Sopu, Andreea. "Psychiatric presentation and somatic complications in anti-glutamic acid decarboxylase (GAD) antibodies." Romanian Journal of Psychiatry and Psychotherapy 26, no. 2 (2024): 43–46. https://doi.org/10.37897/rjpp.2024.2.3.

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Autoimmune encephalitis is a rapidly evolving group of immune-mediated disorders characterized by brain inflammation and neuropsychiatric symptoms, caused by antibodies targeting neuronal cell surface proteins, ion channels, or receptors. Among the involved antigens, autoantibodies against NMDAR, AMPAR, GAD, GABA-AR/BR, LGI1, CASPR2, mGluR5, DPPX, and Neurexin-3a play significant roles in the pathogenesis of autoimmune encephalitis (AE) in adults. Glutamic acid decarboxylase (GAD), particularly its isoform GAD65, is a key enzyme in GABA production, and its antibodies are associated with condit

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Hadi, Hiba Ali Al-Khadhi, Hayam Khalis Al-Masoudi, and Mohammed Salih Mahdi. "The association between anti-glutamic acid decarboxylase IgG and hemoglobin A1C among newly diagnosed type 1 diabetes of some Iraqi children in Karbala City." Medical Journal of Babylon 20, no. 4 (2023): 705–8. http://dx.doi.org/10.4103/mjbl.mjbl_72_23.

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Abstract Background: Type 1 diabetes mellitus (T1DM) is brought on by immune system dysfunction intolerance, invasion of beta cells by autoreactive immunological T cells, degradation of beta cell activity and survival, and extended exogenous insulin treatment. One of the circulation autoantibodies against antigens of pancreatic cell that produce insulin is glutamic acid decarboxylase (GAD IgG antibody) that indicate the stress and/or death of the islet cell in T1D. A blood glucose monitoring test called hemoglobin A1C (HbA1c) is used to determine the average blood sugar level over three months

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Sopu, Andreea. "Psychiatric presentation and somatic complications in anti-glutamic acid decarboxylase (GAD) antibodies: A case report." Romanian Journal of Psychiatry and Psychotherapy 24, no. 4 (2022): 105–8. http://dx.doi.org/10.37897/rjpp.2022.4.3.

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Autoimmune encephalitis represents a rapidly evolving group of immune-mediated disorders characterized by brain inflammation and neuropsychiatric symptoms, resulting from antibodies targeting neuronal cell surface proteins, ion channels, or receptors. Among the antigens involved, autoantibodies against NMDAR, AMPAR, GAD, GABA-AR/BR, LGI1, CASPR2, mGluR5, DPPX, and Neurexin-3a are significant in the pathogenesis of autoimmune encephalitis (AE) in adults. Glutamic acid decarboxylase (GAD), specifically its isoform GAD65, is a key enzyme in the production of GABA, and its antibodies are associate

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