PMID- 11353444
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20190906
IS  - 0148-7299 (Print)
IS  - 0148-7299 (Linking)
VI  - 105
IP  - 3
DP  - 2001 Apr 8
TI  - Linkage study of polymorphisms in the gene for myelin oligodendrocyte 
      glycoprotein located on chromosome 6p and attention deficit hyperactivity 
      disorder.
PG  - 250-4
AB  - Family and twin studies have shown that there is a substantial genetic 
      contribution to both reading disabilities (RD) and attention deficit 
      hyperactivity disorder (ADHD), and recent twin studies have suggested that the 
      overlap between these phenotypes is largely due to common genetic influences. 
      Studies using a linkage approach to search for genes for susceptibility to RD and 
      ADHD have identified regions linked to each of these phenotypes separately, with 
      recent studies suggesting that some chromosomal regions may contribute to both. 
      Linkage to the human leukocyte antigen (HLA) region has been targeted in 
      particular for RD and ADHD, as both of these disorders have been suggested to be 
      autoimmune. Linkage to the HLA region of 6p for RD has now been reported by 
      several groups. Alleles at two genes in the HLA (C4B and DRB1) have also been 
      reported to be associated with ADHD, prompting one investigator to suggest a 
      possible connection between the linkage of RD and ADHD to this region. The 
      location of the gene for myelin oligodendrocyte glycoprotein (MOG), in the region 
      of 6p with the strongest evidence for linkage to RD, and its proposed role as a 
      minor component of myelin in the central nervous system suggest that it may be a 
      factor in neuronal functioning and therefore a candidate for RD and ADHD. In this 
      study, we tested the gene for linkage to ADHD by genotyping two polymorphisms in 
      the MOG gene-a dinucleotide repeat located upstream from the MOG transcription 
      start site and a Val145Ile substitution in exon 3-in a sample of 104 nuclear 
      families identified through a proband with ADHD. We examined the transmission of 
      the alleles of the Val145Ile and the dinucleotide repeat polymorphisms using the 
      transmission disequilibrium test. We did not observe biased transmission of the 
      alleles at either polymorphism to ADHD probands or siblings. Our findings using 
      this sample do not support the role of the MOG gene in ADHD.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Barr, C L
AU  - Barr CL
AD  - Department of Psychiatry, Toronto Western Hospital, University Health Network, 
      Toronto, Ontario, Canada. cbarr@uhnres.utoronto.ca
FAU - Shulman, R
AU  - Shulman R
FAU - Wigg, K
AU  - Wigg K
FAU - Schachar, R
AU  - Schachar R
FAU - Tannock, R
AU  - Tannock R
FAU - Roberts, W
AU  - Roberts W
FAU - Malone, M
AU  - Malone M
FAU - Kennedy, J L
AU  - Kennedy JL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Med Genet
JT  - American journal of medical genetics
JID - 7708900
RN  - 0 (MOG protein, human)
RN  - 0 (Myelin Proteins)
RN  - 0 (Myelin-Associated Glycoprotein)
RN  - 0 (Myelin-Oligodendrocyte Glycoprotein)
SB  - IM
MH  - Amino Acid Substitution
MH  - Attention Deficit Disorder with Hyperactivity/*genetics
MH  - Chi-Square Distribution
MH  - Chromosomes, Human, Pair 6/*genetics
MH  - Dinucleotide Repeats
MH  - Dyslexia/genetics
MH  - Gene Frequency
MH  - *Genetic Linkage
MH  - Genetic Testing
MH  - Genotype
MH  - Humans
MH  - Linkage Disequilibrium
MH  - Myelin Proteins
MH  - Myelin-Associated Glycoprotein/*genetics
MH  - Myelin-Oligodendrocyte Glycoprotein
MH  - Nuclear Family
MH  - Polymorphism, Genetic/*genetics
EDAT- 2001/05/16 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/05/16 10:00
PHST- 2001/05/16 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/05/16 10:00 [entrez]
AID - 10.1002/ajmg.1302 [pii]
AID - 10.1002/ajmg.1302 [doi]
PST - ppublish
SO  - Am J Med Genet. 2001 Apr 8;105(3):250-4. doi: 10.1002/ajmg.1302.