RE: Magnetic resonance spectroscopy of the brain: review of metabolites and clinical applications

摘要

Sir-The article by Soares1 states that it is useful to note that creatine itself does not originate in the brain, quoting evidence that brain creatine levels are altered by renal disease, and that creatine has been noted to be absent in some inborn errors of creatine synthesis, which are subsequently corrected by creatine supplementation. In contrast, it is well established that the brain has all the necessary synthetic machinery to make creatine. The two main enzymes for creatine synthesis are present in both neurons and glia. The brain derives much of its creatine via this synthetic pathway but is also capable of taking creatine up from the blood via a sodium-dependent transporter, which also transports the immediate synthetic precursor guanidinoacetate. It has been suggested that creatine synthesis in the brain largely occurs in a cycle between cell types, which may explain why some inborn errors of transporter deficiency present with little brain creatine; the lack of the transporter means that the synthetic precursor guanidinoacetate is also unable to move between cell types. Arginine is one of the precursor amino acids for creatine synthesis and the level of arginine is subject to fluctuation by renal disease as it is sensitive to ammonia levels.