Port, John D.

ObjectivesThe aim of the present study was to examine N‐acetylaspartate (NAA), a general marker of neuronal viability, and total NAA (tNAA), the combined signal of NAA and N‐acetylaspartylglutamate, in bipolar depression before and after lamotrigine treatment. Given that NAA is synthesized through direct acetylation of aspartate by acetyl‐coenzyme A‐l‐aspartate‐N‐acetyltransferase, we hypothesized that treatment with lamotrigine would be associated with an increase in NAA level.MethodsPatients with bipolar depression underwent two‐dimensional proton magnetic resonance spectroscopy of the anterior cingulate at baseline (n = 15) and after 12 weeks of lamotrigine treatment (n = 10). A group of age‐matched healthy controls (n = 9) underwent scanning at baseline for comparison.ResultsAt baseline, patients with bipolar depression had significantly lower NAA [mean standard deviation (SD) = 1.13 (0.21); p = 0.02] than controls [mean (SD) = 1.37 (0.27)]. Significant increases in NAA [mean (SD) = 1.39 (0.21); p = 0.01] and tNAA [mean (SD) = 1.61 (0.25); p = 0.02] levels were found after 12 weeks of lamotrigine treatment.ConclusionsThese data suggest an NAA deficit in bipolar depression that is normalized after lamotrigine treatment. Future research is warranted to evaluate whether baseline NAA level is a potential biomarker for identifying lamotrigine response patterns and whether this functional brain change has an associated clinical response.

Despite advances in understanding the roles of adiposity, food intake, GI and adipocyte-related hormones, inflammatory mediators, the gut–brain axis and the hypothalamic nervous system in the pathophysiology of obesity, the effects of different therapeutic interventions on those pathophysiological mechanisms are controversial. There are still no low-cost, safe, effective treatments for obesity and its complications. Currently, bariatric surgical approaches targeting the GI tract are more effective than non-surgical approaches in inducing weight reduction and resolving obesity-related comorbidities. However, current guidelines emphasise non-surgical approaches through lifestyle modification and medications to achieve slow weight loss, which is not usually sustained and may be associated with medication-related side effects. This review analyses current central, peripheral or hormonal targets to treat obesity and addresses challenges and opportunities to develop novel approaches for obesity.

Proton magnetic resonance spectroscopy (1H‐MRS) is a safe, noninvasive way of quantifying in vivo biochemical and metabolite concentration levels in individuals withAutismSpectrumDisorders (ASD). Findings to date suggestASDis associated with widespread reduction inN‐acetylaspartate (NAA), creatine plus phosphocreatine (Cr), choline‐containing compounds (Cho),myo‐inositol (mI), and glutamate plus glutamine plus gamma‐Aminobutyric Acid (Glx); however, variable findings, and even substantial increases, are not uncommon depending on the study and/or region‐of‐interest. Widespread reduction ofNAA,Cr,Cho,mI, andGlxinASDlikely reflects impaired neuronal function and/or metabolism related to abnormal neurodevelopmental processes. Future studies should attempt to relate1H‐MRSfindings to histological findings and control for variability in subject age and functioning level; this would assist in evaluating the relationship between1H‐MRSmetabolic levels and neuronal and glial cell densities, as well as neurodevelopmental process associated withASD. Furthermore, more longitudinal1H‐MRSstudies are needed in both control andASDsubjects to attempt to standardize metabolite levels across different developmental periods in well‐defined endophenotypes. This will provide for a standard rubric for which metabolic aberrations (as well as treatment responses) can be measured. With higher magnetic field strengths and spectral‐editing techniques capable of quantifying less‐concentrated metabolites,1H‐MRSwill continue to be an important tool inASDresearch.Autism Res2013, 6: 119–133.© 2013 International Society for Autism Research, Wiley Periodicals, Inc.