I obtained my Masters degree in Biochemistry, from the Bangalore University in the year 2009, after which I worked as a Junior Research Fellow at Indian Institute of Science, Bangalore for about one year. There, I carried out routine molecular biology and protein purification work.

My scientific interests gained fresh impetus when I was recruited as a ‘Biochemist’ (2011-2012) at NIMHANS, Bangalore to study antipsychotic induced metabolic abnormalities in patients with schizophrenia. In this study we prospectively followed up untreated patients with schizophrenia in a rural South Indian community for 12 months after starting antipsychotics according to standard treatment guidelines and examine the incidence and determinants of metabolic adverse effects of treatment. Antipsychotic induced complications like Obesity, Insulin Resistance, Dyslipedemia could be caused in various ways one of which is receptor antagonism, which may have correlation with particular variant (SNP). Hence we studied (a) -759C/T Polymorphism of 5HT2C receptors; (b) -2548G/A Polymorphism of Leptin gene; (c) -1291C/G Polymorphism of alpha2-adrenergic receptors by PCR-RFLP based genotyping as there is evidence of their involvement in antipsychotic induced metabolic complications.

Later I was enrolled in the Ph. D programme in Psychiatry, NIMHANS (Dec, 2012). As a part of my Ph. D Thesis, titled, “Parental consanguinity and its association with metabolic abnormality in patients with schizophrenia: A clinical and genetic investigation”, I have studied different aspects of genetics and metabolic abnormalities in community dwelling patients with schizophrenia. The exact mechanism of development of metabolic abnormalities in the patients remains poorly understood. Nevertheless, genetic factors undoubtedly play an important causal role (in addition to the role of antipsychotics, diet and other lifestyle related factors). Emerging evidence, indicate that parental consanguineous marriage is a risk factor for schizophrenia. Earlier studies support a model of highly polygenic inheritance characterized by small cumulative effects of many risk alleles but the exact inherited risk factors and the mechanism remains obscure. Another important finding reported in earlier studies is the association between parental consanguinity and complex disorders like diabetes. Given these associations, we attempted to explore the link between parental consanguinity and metabolic abnormalities in patients with schizophrenia. As a methodology for assessment of parental consanguinity, we used genome wide genetic variants (N=384 Autosomal SNPs, LD, r2 < 0.9) to calculate coefficients of

inbreeding ‘f’. Parental consanguinity was defined by ‘f’≥ 0.0156. ‘f’ was compared between extreme phenotypes; affected (schizophrenia) and unaffected (no psychotic disorder) Individuals. The SNPs used for this study were based on the HapMap database (GIH) and had been selected by pruning for independence (VIF around 1), excluding SNPs with MAF < 0.3. We used Fluidigm EP1 SNP type assay. Fluidigm SNP Genotyping Analysis software was used to view results after automated genotype clustering and calling. PLINK, version 1.9 was used for quality control procedure and calculation of ‘f’.

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