N-acetyl-aspartate supplement

N-Acetylaspartate, or N-acetylaspartic acid, is a derivative of aspartic acid and the most concentrated molecule in the brain after the amino acid glutamate. N-acetyl-aspartate is synthesized in neurons from the amino acid aspartate and acetyl-coenzyme A.

As of 2010, no human studies with N-Acetylaspartate supplements could be found on Medline so we don't know the proper dosage and benefits or side effects.

N-acetyl-aspartate role in brain tissue
N-Acetylaspartate functions in the brain as a source of acetate for lipid and myelin synthesis in oligodendrocytes, the glial cells that myelinate neuronal axons and a contributor to energy production from the amino acid glutamate in neuronal mitochondria.

N-acetyl-aspartate levels in brain related to obesity
Middle-aged people who are overweight or obese have lower levels of N-acetyl-aspartate and brain chemicals that signal good brain health and function. Dr. Stefan Gazdzinski of the San Francisco VA Medical Center looked at magnetic resonance imaging (MRI) brain scans from 50 healthy middle-aged men and women, measuring amounts of a variety of chemicals in the white and gray matter of the brain. Five of the study participants were obese, 15 were overweight, and the remaining 30 were normal weight. The higher a person's body mass index (BMI), the lower the concentration of N-acetyl-aspartate, a brain chemical that serves several functions and also acts as a marker for overall brain health, in the white matter of the brain's frontal, temporal and parietal regions. Heavier people also had less N-acetyl-aspartate in their frontal gray matter, and lower concentrations of choline-containing metabolite -- substances key to the formation of cell membranes--in their frontal white matter. The data didn't allow Dr. Stefan Gazdzinski to determine if the brain abnormalities might be related to body fat alone or if it suggests other health problems, nutrition, or sedentary living. Annals of Neurology, 2008.

Information benefit and side effects with future studies

Transient alterations of creatine, creatine phosphate, N-acetylaspartate and high-energy phosphates after mild traumatic brain injury in the rat.
Mol Cell Biochem. 2009. Signoretti S, Di Pietro V, Vagnozzi R, Belli A, D'Urso S, Tavazzi B. Division of Neurosurgery, Department of Neurosciences-Head and Neck Surgery, "San Camillo" Hospital, Rome, Italy.
In this study, the concentrations of creatine (Cr), creatine phosphate (CrP), N-acetylaspartate, ATP, ADP and phosphatidylcholine (PC) were measured at different time intervals after mild traumatic brain injury (mTBI) in whole brain homogenates of rats. Anaesthetized animals underwent to the closed-head impact acceleration "weight-drop" model (450 g delivered from 1 m height = mild traumatic brain injury) and were killed at 2, 6, 24, 48 and 120 h after the insult (n = 6 for each time point). Sham-operated rats were used as controls. Compounds of interest were synchronously measured by HPLC in organic solvent deproteinized whole brain homogenates. A reversible decrease of all metabolites but PC was observed, with minimal values recorded at 24 h post-injury (minimum of CrP = 48 h after impact). In particular, Cr and NAA showed a decrease of 44.5 and 29.5%, respectively, at this time point. When measuring NAA in relation to other metabolites, as it is commonly carried out in "in vivo" (1)H-magnetic resonance spectroscopy ((1)H-MRS), an increase in the NAA/Cr ratio and a decrease in the NAA/PC ratio was observed. Besides confirming a transient alteration of N-acetylaspartate homeostasis and ATP imbalance, our results clearly show significant changes in the cerebral concentration of Cr and CrP after mTBI. This suggests a careful use of the N-acetylaspartate /Cr ratio to measure NAA by (1)H-MRS in conditions of altered cerebral energy metabolism. Our data suggest that, under pathological conditions affecting the brain energetic, the Cr-CrP system is not a suitable tool to buffer possible ATP depletion in the brain, thus supporting the growing indications for alternative roles of cerebral Cr.