| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Acid maltase; GAA; Glucosidase alpha acid; LYAG;;Lysosomal alpha glucosidase |
| WB Predicted band size | Calculated MW: 105 kDa ; Observed MW: 120,100,75 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat |
| Immunogen | A synthesized peptide derived from human Lysosomal alpha glucosidase |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol. |
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以下是关于GAA抗体(谷氨酸脱羧酶抗体，GAD抗体)的3篇经典文献和1篇方法学研究的简要总结：
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1. **文献名称**：Identification of the 64K autoantigen in type 1 diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase
**作者**：Baekkeskov, S., et al.
**摘要**：该研究于1990年首次证实，1型糖尿病患者体内靶向胰腺β细胞的64K自身抗原是谷氨酸脱羧酶(GAD65)。GAD抗体的发现为1型糖尿病的自身免疫机制提供了关键证据，并成为该疾病的重要生物标志物。
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2. **文献名称**：Autoantibodies to glutamic acid decarboxylase in a patient with stiff-man syndrome, epilepsy, and type I diabetes mellitus
**作者**：Solimena, M., et al.
**摘要**：此研究(1988年)报道了GAD抗体与僵人综合征(一种罕见神经系统疾病)的关联，同时发现部分患者合并1型糖尿病。结果表明GAD抗体可能同时攻击中枢神经系统和胰腺β细胞，提示自身免疫反应的广泛性。
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3. **文献名称**：Glutamic acid decarboxylase and diabetes: where are we now?
**作者**：Lernmark, Å.
**摘要**：这篇综述(发表于*Diabetes*期刊)系统总结了GAD抗体在1型糖尿病预测、诊断和分型中的临床意义，并探讨其与其他自身免疫疾病(如自身免疫性多内分泌综合征)的潜在关联。
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4. **文献名称**：Autoantibodies to glutamic acid decarboxylase detected by a two-site immunoradiometric assay
**作者**：Grubin, C.E., et al.
**摘要**：研究团队于1994年开发了一种高灵敏度的双位点免疫放射分析法(IRMA)，用于检测GAD抗体。该方法显著提高了1型糖尿病和神经系统疾病患者中GAD抗体检测的特异性和效率。
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如需具体DOI或补充更多近期研究(如GAD抗体在LADA糖尿病中的作用)，可进一步说明研究方向。
**Background of GAA Antibodies**
Glutamic acid decarboxylase (GAD) antibodies, sometimes referred to as GAA antibodies (anti-GAD antibodies), are autoantibodies targeting the enzyme glutamic acid decarboxylase, which catalyzes the conversion of glutamate to gamma-aminobutyric acid (GABA), a key inhibitory neurotransmitter. First identified in the 1980s, these antibodies are strongly associated with autoimmune disorders, particularly type 1 diabetes (T1D) and neurological conditions like stiff-person syndrome (SPS). In T1D, anti-GAD antibodies contribute to the destruction of pancreatic beta cells, serving as a diagnostic marker alongside other islet autoantibodies. In SPS, they are linked to impaired GABAergic signaling, leading to muscle rigidity and spasms.
Anti-GAD antibodies are detected via immunoassays (e.g., ELISA, radioimmunoassay) and are present in 70-80% of T1D patients at diagnosis. Their role extends beyond diagnostics; elevated titers may correlate with disease progression or specific clinical subtypes. Research also explores their presence in other conditions, including cerebellar ataxia and epilepsy, though mechanisms remain unclear. While their pathogenic role is debated (markers vs. direct effectors), they remain critical in understanding autoimmune pathogenesis and guiding personalized treatments, such as immunotherapy in neurological cases. Ongoing studies aim to clarify their biological impact and therapeutic implications.
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