OADES, R. D., Dauvermann, M.R., Schwarz, M. J., & Myint, A. M., Does glial function underlie ADHD variability? Evidence from measures of S100B, interleukins, tryptophan metabolism and the kynurenine metabolic pathway. 10th Psychoimmunology Expert Meeting, Ulm/Günzburg, Nov. 12-14):
Neurology, Psychiatry and Brain Research, suppl. 1, 44.

Objectives: Response variability is a core feature of ADHD. A deficient supply of energy from astrocytes to support sustained neural activity may underlie this characteristic (1). We report a measure of the integrity of glial function (the neurotrophin S100B) and on measures of tryptophan metabolism (kynurenine pathway) where toxic metabolites could induce dysfunction (2). We also considered 8 interleukins/cytokines where the balance of pro/anti-inflammatory elements bias metabolism to neuroprotective or potentially toxic products. We predicted low S100B activity in ADHD where increased levels characterise psychosis and dementia (3).

Methods: We compared 21 young medication-naïve ADHD-ct children with 21 healthy controls, 14 patients on medication and 7 siblings. All patients demonstrated variability on a Qb test. Serum was analysed for S100B, IL-1ß, IL-2, IL-6, IL-10, IL-13, IL-16, TNFa and IFNy; for 17 amino acids, kynurenine, kynurenate and 3-hydroxykynurenine (3HK).

1 - There were no group differences for levels of S100B. However decreasing levels related to increasing internalizing symptoms (e.g. anxiety) in the patients.

2 - There were no clear group differences for the interleukins. But, medication tended to normalise the alterations recorded.

3 - The positive/negative relationships of IL-16/IL-10 to allergy sensitivity were modulated by oppositional/hyperactive symptoms.

4 - Lastly, levels of the potentially toxic 3HK were higher in controls than patients. The implied increase of catabolism was supported by associations with amino acid levels not seen in the patients.

Discussion: 1/ Our hypothesis of decreased S100B levels in ADHD children was not supported. But other markers of glial function should be examined (e.g. myo-inositol, LIF). 2/ The modest immunological imbalance (interleukins) was positively influenced by stimulant medication. This indicates a neglected glial source (and target) for therapeutic effects. 3/ Increased toxic metabolite activity in typically developing children rather than the patients was not anticipated. This may reflect normal pruning activity in the CNS in late childhood (4) which appears to be reduced or delayed in the ADHD children.

1) Russell, Oades, Tannock et al (2006) Behav Brain Funct 2: 30:
2) Myint, Kim, Verkerk et al (2007) J Affect Disord, 98, 143-151:
3) Schwarz, Riedel, Holdenrieder et al 2008 In Vivo, 21, 951:
4) Huttenlocher (1984) Am J Ment Defic Res, 88, 488-496:
The study was supported by the UCB GmbH. We thank Victoria Kirchhoff and Ellen Uslar for assistance.