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Radhakrishna Vakkalanka

Researcher at National Institutes of Health

Publications -  25
Citations -  2752

Radhakrishna Vakkalanka is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Psychosis & Schizophrenia. The author has an hindex of 22, co-authored 25 publications receiving 2621 citations. Previous affiliations of Radhakrishna Vakkalanka include Johns Hopkins University & United States Department of Health and Human Services.

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Genetic variation in CACNA1C affects brain circuitries related to mental illness

TL;DR: The risk-associated single-nucleotide polymorphism in CACNA1C maps to circuitries implicated in genetic risk for bipolar disorder and schizophrenia, and its effects in human brain expression implicate a molecular and neural system mechanism for the clinical genetic association.
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Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression.

TL;DR: Quantitative transmission disequilibrium test analyses revealed that variation in GAD1 influenced multiple domains of cognition, including declarative memory, attention and working memory, and suggest that the mechanism involves altered cortical GABA inhibitory activity, perhaps modulated by dopaminergic function.
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GAD1 (2q31.1), which encodes glutamic acid decarboxylase (GAD67), is associated with childhood-onset schizophrenia and cortical gray matter volume loss.

TL;DR: Quantitative trait TDT analyses showed an intriguing association between several SNPs and increased rate of frontal gray matter loss, suggesting that the gene encoding GAD67 may be a common risk factor for schizophrenia.
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Serious obstetric complications interact with hypoxia-regulated/vascular-expression genes to influence schizophrenia risk.

TL;DR: Although the sample size was modest and the power to detect interactions was limited, significant evidence is reported for genes involved in neurovascular function or regulated by hypoxia interacting with the presence of serious obstetric complications to increase risk for schizophrenia.
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DISC1 splice variants are upregulated in schizophrenia and associated with risk polymorphisms.

TL;DR: The results implicate a molecular mechanism of genetic risk associated with DISC1 involving specific alterations in gene processing, and suggest that truncated DISC 1 proteins were expressed more abundantly during fetal development than during postnatal ages.