Table 1.

Candidate genes with their biological effects and functional effects.

Gene	Biological effect	Functional effect
APOE	The ε4 haplotype reduces acetylcholine receptor number (Parasuraman et al., 2002) and possibly diminishes synthesis of acetylcholine via impaired regulation of phospholipid and/or fatty acid transport (Poirier, 1996).	APOE has been associated with visuospatial skills in children (Bloss et al., 2010) and appears to have a protective role in cognitive development (Oriá et al., 2010).
BDNF	This gene is involved in the serotonergic system (Juckel et al., 2010) as well as nerve growth (Nair and Mishra, 1995).	Related to impulsive-aggressive behaviors in children (Oades et al., 2008).
CHRNA4	This gene encodes a nicotinic acetylcholine receptor that can bind acetylcholine and open an ion-conducting channel across the plasma membrane. The protein can interact with either nAChR beta-2 or nAChR beta-4 to form a functional receptor (Winterer et al., 2007).	Associated to with ADHD in children (Faraone and Mick, 2010)
COMT	G at rs4680 produces valine which is more active in catabolizing dopamine making dopamine less available (Axelrod and Tomchick, 1958).	COMT has been associated with working memory and brain activity during development (Dumontheil et al., 2011).
DRD4	Risk alleles lead to fewer dopamine receptors via reduced transcription (Lowe et al., 2004).	There is an association between DRD4, cortical development, and ADHD (Shaw et al., 2007).
HTR4	A member of the family of serotonin receptors; the gene product modulates various neurotransmitters (Lambe et al., 2011).	Associated with depression, autism, and ADHD (Faraone and Mick, 2010).
IGF2	This gene encodes a member of the insulin family of polypeptide growth factors, which are involved in development (including DA neuron development) and growth (Riikonen et al., 2010). It is an imprinted gene, expressed only from the paternal allele (Kopsida et al., 2011).	Epigenetic changes at this locus are associated with developmental growth disorders such as Beckwith-Wiedemann syndrome (Nativio et al., 2011). Normal intelligence is possible if long term neonatal hypoglycemia is avoided (Obias et al., 1992).
MAOA	This gene is on chromosome X. It encodes an enzyme that degrades amine neurotransmitters, such as dopamine and serotonin (Xu et al., 2007).	Abnormal regulation of MAOA has been associated with depression, substance abuse, and sexual maturation (Biederman et al., 2008).
SLC5A7 (aka CHT)	The presynaptic choline transporter (CHT, SLC5A7) is the major rate-limiting determinant of ACh production in the brain and periphery (Neumann et al., 2005).	Upregulated during tasks that require sustained attention (English et al., 2009).
SLC6A3(aka DAT1)	Controls the number of dopamine transporter and therefore less dopamine in the synapse (Giros et al., 1992) and this terminates the dopaminergic signal transmission (Rommelse et al., 2008).	Less dopamine has been associated with greater attentional costs for targets in the left hemifield of children (Bellgrove et al., 2007).
SNAP25	This gene product is a presynaptic plasma membrane protein involved in the regulation of neurotransmitter release, including dopamine (Feng et al., 2005).	SNAP25 has been associated with ADHD (Feng et al., 2005).

Note: Biological effects include changes to the gene that alter the way the protein it codes for is produced (e.g., changes in a synaptic receptor, enzyme, or neurotransmitter). Function effects include associations between this genetic variation and behaviors, including symptoms of disorders associated with attention.