Month: april 2018

Introduction: Attention-deficit hyperactivity disorder (ADHD) is one of the most frequent neurodevelopmental disorders in children and tends to persist into adulthood. Evidence from neuropsychological, neuroimaging, and electrophysiological studies indicates that alterations of error processing are core symptoms in children and adolescents with ADHD. To test whether adults with ADHD show persisting deficits and compensatory processes, we investigated performance monitoring during stimulus-evaluation and response-selection, with a focus on errors, as well as within-group correlations with symptom scores.

Methods: Fifty-five participants (27 ADHD and 28 controls) aged 19–55 years performed a modified flanker task during EEG recording with 64 electrodes, and the ADHD and control groups were compared on measures of behavioral task performance, event-related potentials of performance monitoring (N2, P3), and error processing (ERN, Pe). Adult ADHD Self-Report Scale (ASRS) was used to assess ADHD symptom load.

Results: Adults with ADHD showed higher error rates in incompatible trials, and these error rates correlated positively with the ASRS scores. Also, we observed lower P3 amplitudes in incompatible trials, which were inversely correlated with symptom load in the ADHD group. Adults with ADHD also displayed reduced error-related ERN and Pe amplitudes. There were no significant differences in reaction time (RT) and RT variability between the two groups.

Conclusion: Our findings show deviations of electrophysiological measures, suggesting reduced effortful engagement of attentional and error-monitoring processes in adults with ADHD. Associations between ADHD symptom scores, event-related potential amplitudes, and poorer task performance in the ADHD group further support this notion.

Original Research ARTICLE:

https://doi.org/10.3389/fpsyg.2018.00485

Elaheh Mahootchi, Arne Raasakka,‡ Ingeborg Winge,^a,b Weisha Luan,^c Petri Kursula^a,c* and Jan Haavik^a,b,d*

^a Department of Biomedicine, University of Bergen, Bergen, Norway, ^b K. G. Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway, ^c Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland, and ^d Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.

‡ These authors made equal contributions

Aims:

Glutamic acid decarboxylase-like protein 1 (GADL1) is a recently discovered pyridoxal 5′-phosphate -dependent enzyme that has been associated with lithium response in bipolar disorder. The expression pattern and activity of GADL1 suggest a role in neurotransmitter and neuroprotectant metabolism, notably in the synthesis of beta-alanine and carnosine in the olfactory bulb. The catalytic properties and crystal structure of mouse GADL1 is described, together with a solution model based on small-angle X-ray scattering data.

Methods:

• Construct preparation, protein expression and purification

• Expression and purification of mouse GADL1 (MmGADL1)

• Crystallization

• Small-angle X-ray scattering

Results:

The substrate specificity and physiological functions of GADL1 are still unclear. While the overall fold and the conformation of the bound PLP are similar to those in other PLP-dependent decarboxylases, GADL1 adopts a more loose conformation in solution, which might have functional relevance in ligand binding and catalysis.

Conclusions:

The structure of MmGADL1 and its flexibility in solution, coupled to structural conservation with other PLP-dependent enzymes, point towards functional relevance of these features within the enzyme family. Future work will concentrate on high-resolution structural details of substrate and inhibitor binding by GADL1, as well as characterization of its metabolic role in mouse tissues.

https://www.ncbi.nlm.nih.gov/pubmed/29372909