PLoS One 2015;10:e0121364. (2/3; 66.66%), and neuropathy (4/7; 57.1%) while women were more with autoimmune encephalitis (6/8; 75%). Eighteen (22.6%) had underlying autoimmunity (three had type 1 diabetes mellitus). Six (7.4%) had underlying neoplasm. Thirty-three out of 43 patients responded to immunotherapy (76.74%). Five had spontaneous improvement. Conclusion: Glutamic acid decarboxylase65 antibody values were much lower in our study population. Male-dominant autoimmunity was seen unlike that in Western literature. The most striking was the high preponderance of atypical parkinsonism in GAD 65-positive patients. We also found that GAD 65 positivity is a useful marker for a positive response to immunotherapy in suspected autoimmune neurological syndromes irrespective of their titers. Keywords: Atypical parkinsonism, autoimmune atypical parkinsonism, autoimmune encephalitis, glutamic acid decarboxylase65 antibody INTRODUCTION Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme to produce gamma-aminobutyric acid, which is the main inhibitory neurotransmitter in S100A4 the central nervous system. It has 2 isoforms GAD 65 and GAD67, of which GAD 65 is used more extensively as a clinical biomarker due to its greater autoantigenicity.[1] It is widely used as a biomarker for type 1 diabetes mellitus, but relatively lately, it is also being used as a marker of neurological autoimmunity.[2] Stiff-person syndrome, limbic encephalitis, epilepsy, cerebellar ataxia, isolated cases of palatal tremor, and paraneoplastic neurological syndromes are some of the neurological diseases in which GAD 65 positivity is described.[3-6] GAD 65 positivity has also been described in multiple system atrophy and some patients with cognitive decline.[7,8] Most of the literature on GAD 65 neurological autoimmunity is from the West. There are only a few studies from Asia on the neurological manifestation of the GAD 65 antibody.[7-11] Sparse data is available on neurological manifestations of GAD 65 autoimmunity in Asians and no data on Indian patients. We present a retrospective case series of GAD 65-positive patients with an intent of identifying the neurological phenotypes in the Indian population. The previous studies in the Western population show that very high values of GAD 65 were seen in neurological autoimmunity compared to endocrine autoimmunity and low values were seen in the normal population as well.[2,3,12-14] METHODS The study was conducted in the department of neurology and biochemistry in Amrita Institute of Medical Sciences, Kochi, Kerala, which is the tertiary care post-graduate teaching hospital in South India. Inclusion criteriaCThose individuals who were tested positive for GAD 65 antibody were included in the study if the request was made for analysis of neurological disease from February 2013 to July 2019. Exclusion criteriaPatients referred from additional countries were excluded. We retrospectively identified patients, who were tested for GAD 65 antibody as per the request of neurologists Alvimopan dihydrate from February 2013 to July 2019 by critiquing electronic medical records (EMR). Clinical and treatment details of positive individuals were extracted from EMR. Levels of GAD 65 antibody were recognized using enzyme-linked immunosorbent assay (ELISA) using commercial kits and following manufacturer’s instructions. Two ELISA diagnostics packages were used to detect levels of GAD 65 antibody during the period between February 2013 to July 2019. Medizym anti-GAD ELISA, (MEDIPAN GMBH, Berlin, Germany) was used from 2013 February to 2016 June; Anti-GAD ELISA (EUROIMMUN AG, Luebeck, Germany) was used from 2016 June to 2019 July. For the 1st ELISA kit >5.0 IU/ml was considered as positive and for the second ELISA kit >10 IU/ml was considered as positive. Clinical results were measured with 9-query modified Rankin Level (mRS-9Q) (reduction in score by a score of one is considered as improvement), Unified Parkinson Disease Rating Level (UPDRS) and Glasgow Coma Level (GCS). All consecutive GAD 65 individuals were included in the study. cerebrospinal fluid (CSF) GAD 65 assay was not performed. Tissue-based assay was performed in all individuals to detect neuronal antibodies. Statistical analysis was performed using IBM SPSS version 20.0 software. Categorical variables were indicated using rate of recurrence and percentage. Numerical variables were offered using mean and standard deviation (SD). To test the statistical significance of the association of two categorical variables, Chi-square test was used. A = 47) outnumbered the females (= 34) [Refer Table 1]. All the GAD ideals measured were below 5000 IU/ml. Thirty-four individuals had a medical Alvimopan dihydrate analysis of atypical parkinsonism (two with coexisting autoimmune encephalitis, one with coexisting myasthenia), eight experienced autoimmune encephalitis, three experienced the stiff-person syndrome, seven experienced neuropathy (including two with atypical GBS and one with CIDP), two experienced Creutzfeldt Jakob disease, two experienced cervical demyelinating Alvimopan dihydrate myelopathy, two experienced motor neuron diseases, two experienced epilepsy one experienced aquaporin 4 IgG-positive neuromyelitis optica syndrome, one experienced myasthenia gravis, one lambert eaton myasthenic syndrome (LEMS),.