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Stichting ADD Nederland
Stichting ADD Nederland werd opgericht in 2006 en heeft ten doel: Het beter bekend maken van ADD - "Het overwegend onoplettend type" Attention Deficit Disorder.


Recent onderzoek naar ADD 2011 - heden

Nederlands onderzoek naar het overwegend onoplettend type Attention Deficit Disorder: Het onderzoek betreft de afstudeeropdracht van Annebeth Hidding, studente HBO-Psychologie aan het Saxion Next, te Deventer. De resultaten van het onderzoek worden verwacht in 2011.
NIEUW: Effects of a restricted elimination diet on the behaviour of children with attention-deficit hyperactivity disorder
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(INCA study): a randomised controlled trial. Pelsser LM, Frankena K, Toorman J, et al. Lancet 05-01-2011; 377: 494-503. /
"Mapping ADHD: From behaviour to biology"
ADHD is the most common child psychiatric disorder, with at least one affected child in every classroom, and a huge economic impact. Children with ADHD and their families are often stigmatized, as the legitimacy of the diagnosis is called into question. My work and that of others has established beyond doubt that ADHD is a heritable, neurobiological disorder. However, we do not yet understand how biological changes lead to changes in behaviour.
I have shown how neuroimaging can be used to map biological pathways from genes to ADHD. In my VIDI-project, I developed a model that there are three separate neurobiological systems that can lead to ADHD (the systems underlying cognitive control, timing and reward processing). My data support that these systems are separate at the biological level and separable at the cognitive level. In this VICI-proposal, I test this model using state-of-the-art cognitive, neuroimaging and genetic approaches. I address the clinical specificity of each subtype in Part 1. I chart the normal development of these systems in Part 2. These are essential steps to bring this knowledge closer to the clinic, where it can benefit affected individuals and their families.
Distinguishing Sluggish Cognitive Tempo From
Attention-Deficit/Hyperactivity Disorder in Adults

Dr. Russell A. Barkley, Ph.D. 2011 Medical University of South Carolina
Abstract beschikbaar: Januari-maart 2011
Genetic Polymorphisms that may affect EF skills differentially in Males and Females
While males benefit from the version of the COMT (catechol-o-methyltransferase) gene that results in higher dopamine levels in prefrontal cortex (PFC), might females benefit from the version of the COMT that clears dopamine from PFC faster?
We expect to replicate previous findings that men homozygous for the Met version of the COMT gene show superior EF.
However, might women homozygous for the Val version of the COMT gene show better EF performance than women homozygous for the Met version, especially during the point in their menstrual cycles when estrogen levels are high?
Might males and females differ in what dosage levels of dopaminergic drugs are most efficacious? Might the efficacious dosage levels differ for a given woman by what point she is in her menstrual cycle? DCN Lab Vancouver Resultaten binnenkort verwacht.
Clinical features of various subtypes of attention deficit hyperactivity disorders in children: Abstract Chen yanzhao, China: "Significant differences in intellectual abilities between ADHD children and normal children. It is a common phenomenon of the intellectual development imbalance in children with ADHD.The intellectual development imbalance is defined as the difference value between performance intelligence quotient (PIQ) and verbal intelligence quotient (VIQ) is greater than one standard deviation(15) in China. Our study suggests that the incidence of imbalance in the ADHD-I group was higher than the other two groups. Imbalance of Intelligence may lead to Learning Disabilities in children".
Methylphenidate normalizes elevated dopamine transporter densities in an animal model of the attention-deficit/hyperactivity disorder combined type, but not to the same extent in one of the attention-deficit/hyperactivity disorder inattentive type.
Neuroscience. 2010 Jun 2;167(4):1183-91. Epub 2010 Mar 6

The spontaneously hypertensive rat (SHR/NCrl) is a validated model of attention-deficit/hyperactivity disorder (ADHD) combined subtype, whereas a recently identified substrain of the Wistar Kyoto rat (WKY/NCrl) is a model of ADHD inattentive subtype. In this study, we first examined the expression of genes involved in dopamine signaling and metabolism in the dorsal striatum and ventral mesencephalon of these two rat strains, as well as three reference control strains (WKY/NHsd, WK/HanTac, and SD/NTac) using quantitative real time RT-PCR. Next, striatal dopamine transporter (DAT) density was determined by ligand binding assay in the two ADHD-like strains at different developmental stages and after methylphenidate treatment. In adult rats, the mRNA expression of DAT and tyrosine hydroxylase was elevated in SHR/NCrl and WKY/NCrl rats compared to control strains, with differences between SHR/NCrl and WKY/NCrl rats also evident. During normal development, changes of striatal DAT densities occurred in both strains with lower densities in WKY/NCrl compared to SHR/NCrl after day 25. Two-weeks methylphenidate treatment during different developmental stages was associated with decreased striatal DAT density in both rat strains compared to the non-treated rats with more pronounced effects followed prepubertal treatment. These results suggest differences in the pathophysiology of the combined versus the predominantly inattentive animal model of ADHD. Finally, treatment with methylphenidate might reduce elevated DAT levels more effectively in the combined subtype especially when applied before puberty.
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