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Hindi Research Article, J Genet Disor Genet Rep Vol: 3 Issue: 1
Evidence that lithium Inhibits Export of N-Acetyl-L-Aspartate from Neurons: A Retrospective Study of Canavan Disease and Bipolar Disorder Patients
| Morris H Baslow* and David N Guilfoyle |
| Nathan S Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA |
| Corresponding author : Morris H Baslow Nathan S Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA Tel: +1-845-398-5471; Fax: +1-845-398-5472 E-mail: baslow@nki.rfmh.org |
| Received: November 22, 2013 Accepted: December 26, 2013 Published: January 03, 2014 |
| Citation: Baslow MH, Guilfoyle DN (2014) Evidence that lithium Inhibits Export of N-Acetyl-L-Aspartate from Neurons: A Retrospective Study of Canavan Disease and Bipolar Disorder Patients. J Genet Disor Genet Rep 3:1. doi:10.4172/2327-5790.1000110 |
Abstract
Evidence that lithium Inhibits Export of N-Acetyl-L-Aspartate from Neurons: A Retrospective Study of Canavan Disease and Bipolar Disorder Patients
Lithium (Li) is an effective treatment for human bipolar disorder (BD) but whose precise mechanism and site of action are unknown. N-acetyl-L-aspartic acid (NAA) is an amino acid synthesized by and maintained at high steady-state levels within neurons from where it is exported to extracellular fluid (ECF) upon depolarization. NAA is the only precursor for N-acetylaspartylglutamate (NAAG), a neurotransmitter synthesized by neurons and also exported to ECF upon depolarization. The physiological function of NAA is as yet unclear but its unique tri-cellular metabolism between neurons, oligodendrocytes (NAA) and astrocytes (NAAG) is vital for normal brain function. Canavan disease (CD) is a rare inborn error in metabolism of NAA where oligodendrocyte aspartoacylase (ASPA) is inactive and NAA cannot be hydrolyzed resulting in its buildup in brain ECF and excretion in urine.
