|Clinical Care & Knowledge on: ADHD, OCD, Tourette's|
Clinical Research is all investigation performed with the help of patients in hospital or other clinical setting. The purpose is generally to improve the diagnostic tools which are yet poor in the field of psychiatric and behavioral diseases. Only by a deeper investigation potency - in the field of biomarker and/or in the field of tomographic imaging - we can hope to promote better definition and hence better detection of the various facets inherent to psychiatric and behavioral diseases. Clinical Care should always be based on UP-to-DATE CLINICAL KNOWLEDGE... EMMA is fully committed to divulge rapidly all novel discoveries in the field of mind and metabolism, with a special regard on ADHD, Obsessive-Compulsive Disorder, and Tourette Syndrome.
Brain Dev. 2012 Sep; 34(8): 667-73. Epub 2011 Dec 16.
Long term clinical course of Tourette syndrome.
Brain Dev. 2007 Aug; 29(7): 413-20. Epub 2007 Feb 05.
Disentangling the effects of Tourette syndrome and attention deficit / hyperactivity disorder on cognitive and behavioral phenotypes.
Apr 28, 2009 - Altered anandamide degradation in attention-deficit / hyperactivity disorder. By: Centonze D., ..., Curatolo P., Maccarrone M. on Neurology.
ADHD : suggested multiple susceptibility genes
Guan et al., Molecular Psychiatry (2009) 14, 546–554 To read click here
Attention deficit hyperactivity disorder (ADHD) is a common childhood-onset behavioral disorder with a definite genetic component. The search for genes predisposing to ADHD has focused on genes involved in the regulation of monoamine systems. In this study, we emphasized genes that underlie various aspects of dopamine, norepinephrine and serotonin neurotransmissions and performed a comprehensive association analysis by screening with 245 single-nucleotide poly-morphisms (SNPs) of 23 candidate genes in a sample of Chinese Han descent. A total of 182 DSM-IV ADHD children and 184 healthy controls were genotyped and analyzed with an average density of one SNP every 6.1 kb. Both single-SNP and multi-marker haplotype analyses were implemented to exploit association signal for ADHD and its diagnostic subtypes. Empirical P-values were derived on the basis of 5000 permutations to evaluate gene-wide significance. MAOA yielded highly suggestive evidence of association (empirical P<0.01, OR=1.94) with ADHD. For inattentive-subtype ADHD, MAOA, DDC and SYP showed suggestive evidence of a quite strong association (empirical P<0.05). ADRA2C achieved suggestive significance (empirical P<0.05) for ADHD combined type.
Additionally, now comes the most interesting news: for six genes (SNAP25, NET1, DBH, CHRNA4, DRD3 and SYT1) we detected one or more SNPs with nominal P-values0.05. This study has identified several genes as promising susceptibility loci for ADHD. Replication efforts and further investigations remain necessary to provide definite proof of association.
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