Relevant bibliographies by topics / Anti-GAD antibody

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Academic literature on the topic 'Anti-GAD antibody'

Author: Grafiati
Published: 5 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Anti-GAD antibody"

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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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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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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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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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Book chapters on the topic "Anti-GAD antibody"

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Nakamura, Shigenobu, Hidekazu Kamei, and Yasuyo Mimori. "Anti-GAD Antibody in Various Neurological Diseases." In GABA: Receptors, Transporters and Metabolism. Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8990-2_6.

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Conference papers on the topic "Anti-GAD antibody"

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Correia Monteiro, Jean Michell, Mateus Cavarzan Lopes, Heitor Furlan Giordano, Diogo Souza Domiciano, and Samuel Katsuyuki Shinjo. "Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome associated with anti-GAD antibody-related limbic encephalitis." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1909.

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Damasceno Júnior, Eustáquio Costa, Isabella Sabião Borges, João Victor Aguiar Moreira, et al. "Successful treatment with rituximab in a refractory Stiffperson syndrome (SPS)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.507.

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Background: SPS is a disorder consisting of rigidity of axial muscles with painful spasms. More than 80 % of SPS patients have high titer antibodies against glutamic acid decarboxylase (GAD). The use of rituximab for the treatment of SPS is a recent therapeutical approach showing promising results. We present a case of SPS treated with rituximab, showing a good and safe response. Case: A 38-year-old female patient presented with a history of rigidity of abdominal and paravertebral muscles associated with painful spasms in lower back region, increased tonus, lumbar lordosis, frequent falls and
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