PMID- 16756026
OWN - NLM
STAT- MEDLINE
DCOM- 20070320
LR  - 20181201
IS  - 0033-2674 (Print)
IS  - 0033-2674 (Linking)
VI  - 40
IP  - 1
DP  - 2006 Jan-Feb
TI  - [Genetic background of ADHD: genes of the serotonergic system, other candidate 
      genes, endophenotype].
PG  - 33-42
AB  - Recent studies have shown that in the aetiology of attention-deficit 
      hyperactivity disorder (ADHD) genetic factors may be of importance. Biochemical 
      and pharmacological studies reveal a connection between abnormalities of 
      dopaminergic, adrenergic and serotonergic system and ADHD. Therefore genes for 
      enzymes synthesizing or degrading proper neurotransmitters, genes for adequate 
      transporters and receptors and genes for other substances, which altered the 
      level of neurotransmitters, are studied. Many authors describe the connection 
      between ADHD development and the synaptosomal-associated protein 25 (SNAP-25) 
      gene. This protein plays a role in catecholamine secretion. Its higher expression 
      is specific for neurones. SNAP-25 gene mutation may change this protein level, 
      function of synapse and neurotransmitters storage. Acetylcholine receptor alpha4 
      subunit gene stimulation increases the dopamine level. Therefore this receptor 
      gene may be important in the aetiology of ADHD studies. Other possible factors in 
      ADHD background are substance influence on brain maturation, including N-methyl-D 
      aspartate glutamate receptor 2A gene polymorphism (GRIN2A) and brain derived 
      neurotrophic factor (BDNF) gene. One of the greatest challenges in studying the 
      genetic basis of psychiatric disorders is to find appropriate ways to define the 
      relevant endophenotype. ADHD often coexists with other psychiatric disorders, 
      including specific developmental disorders, conduct disorders, 
      obsessive-compulsive disorder and early onset of bipolar disorder.
FAU - Slopien, Agnieszka
AU  - Slopien A
AD  - Klinika Psychiatrii Dzieci i Mlodziezy AM w Poznaniu.
FAU - Dmitrzak-Weglarz, Monika
AU  - Dmitrzak-Weglarz M
FAU - Rybakowski, Filip
AU  - Rybakowski F
FAU - Rajewski, Andrzej
AU  - Rajewski A
FAU - Hauser, Joanna
AU  - Hauser J
LA  - pol
PT  - Journal Article
PT  - Review
TT  - Udzial czynnikow genetycznych w etiologii ADHD. Geny ukladu serotoninergicznego, 
      pozostale geny kandydujace, endofenotyp.
PL  - Poland
TA  - Psychiatr Pol
JT  - Psychiatria polska
JID - 0103314
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Receptors, Nicotinic)
RN  - 0 (Receptors, Serotonin)
RN  - 0 (SNAP25 protein, human)
RN  - 0 (Synaptosomal-Associated Protein 25)
RN  - 0 (nicotinic acetylcholine receptor alpha4 subunit)
RN  - VH92ICR8HX (N-methyl D-aspartate receptor subtype 2A)
SB  - IM
MH  - Attention Deficit Disorder with Hyperactivity/*genetics/metabolism
MH  - Child
MH  - Genetic Predisposition to Disease/genetics
MH  - Humans
MH  - *Phenotype
MH  - Polymorphism, Genetic/*genetics
MH  - Receptors, N-Methyl-D-Aspartate/metabolism
MH  - Receptors, Nicotinic/metabolism
MH  - Receptors, Serotonin/metabolism
MH  - Synaptosomal-Associated Protein 25/metabolism
RF  - 34
EDAT- 2006/06/08 09:00
MHDA- 2007/03/21 09:00
CRDT- 2006/06/08 09:00
PHST- 2006/06/08 09:00 [pubmed]
PHST- 2007/03/21 09:00 [medline]
PHST- 2006/06/08 09:00 [entrez]
PST - ppublish
SO  - Psychiatr Pol. 2006 Jan-Feb;40(1):33-42.