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https://www.selleckchem.com/products/mmri62.html Gyrate Atrophy (GA) of the choroid and retina (MIM# 258870) is an autosomal recessive disorder due to mutations of the OAT gene encoding ornithine-delta-aminotransferase (OAT), associated with progressive retinal deterioration and blindness. The disease has a theoretical global incidence of approximately 11,500,000. OAT is mainly involved in ornithine catabolism in adults, thus explaining the hyperornithinemia as hallmark of the disease. Patients are treated with an arginine-restricted diet, to limit ornithine load, or the administration of Vitamin B6, a precursor of the OAT coenzyme pyridoxal phosphate. Although the clinical and genetic aspects of GA are known for many years, the enzymatic phenotype of pathogenic variants and their response to Vitamin B6, as well as the molecular mechanisms explaining retinal damage, are poorly clarified. Herein, we provide an overview of the current knowledge on the biochemical properties of human OAT and on the molecular, cellular, and clinical aspects of GA.According to the National Center for Health Statistics, the age-adjusted suicide rate in the United States has increased by 33% from 1999 to 2017, and the largest increases are among female individuals aged 10 to 14 years (240% increase) and 15 to 24 years (93% increase).1 Currently, suicide is the second leading cause of death for youths aged 10 to 24 nationally. Decades of studies have noted that the most consistent predictors of death by suicide are previous self-injurious thoughts and behaviors (SITBs), which are disproportionately elevated among Black and Latinx youths. In response, robust efforts have been mobilized to reduce youth suicide, including National Institute of Mental Health (NIMH) funding for several Zero Suicide Studies, with the aims of reducing suicide for individuals receiving treatment within health care systems. More recently, in 2019, the NIMH generated a report for Identifying Research Priorities in Ch

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