Linked Life Data

21184584

Source:http://linkedlifedata.com/resource/pubmed/id/21184584

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-12-24
pubmed:abstractText
Nail-Patella syndrome (NPS) is an autosomal dominant disorder that is the result of heterozygous loss-of-function mutations in LMX1B, coding for a LIM homeobox (LIM-HD) transcription factor. Analyses of lmx1b mutant mice have revealed the role of Lmx1b in the development of mesencephalic dopaminergic neurons and the serotonergic system; these areas have been linked with symptoms of attention deficit hyperactivity disorder (ADHD) and major depressive disorder (MDD). Fifty adults (38 females, 12 males) with NPS completed the Conners' Adult ADHD Rating Scales-Self-report: Long Version (CAARS) and Beck Depression Inventory-II (BDI-II). The objective was to describe the neurobehavioral phenotype of these subjects and examine possible relationships between neurobehavioral symptoms and NPS. Elevated levels of DSM-IV-TR ADHD Inattentive symptoms were reported on the CAARS by 22% of the NPS sample. The BDI-II Total score was elevated for 40% of the NPS sample. There was a significant increase in the odds of an elevated BDI-II Total score when any of the three CAARS scales were elevated (odds ratios ranging from 11.455 to 15.615). The CAARS and BDI-II did not significantly differ with gender, age, or education level. There was no significant association between genetic mutation-predicted protein status and elevations on CAARS or BDI-II. Individuals with NPS reported co-occurring symptoms of ADHD and MDD, with higher levels of co-occurrence than reported in the literature for the general population. The co-occurrence of these symptoms may be related to mesencephalic dopaminergic neurologic pathway abnormalities that are a consequence of LMX1B loss of function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1552-485X
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
156B
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-66
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:21184584-Adult, pubmed-meshheading:21184584-Aged, pubmed-meshheading:21184584-Animals, pubmed-meshheading:21184584-Attention Deficit Disorder with Hyperactivity, pubmed-meshheading:21184584-DNA Mutational Analysis, pubmed-meshheading:21184584-Demography, pubmed-meshheading:21184584-Depressive Disorder, Major, pubmed-meshheading:21184584-Education, pubmed-meshheading:21184584-Female, pubmed-meshheading:21184584-Genetic Predisposition to Disease, pubmed-meshheading:21184584-Homeodomain Proteins, pubmed-meshheading:21184584-Humans, pubmed-meshheading:21184584-LIM-Homeodomain Proteins, pubmed-meshheading:21184584-Male, pubmed-meshheading:21184584-Mice, pubmed-meshheading:21184584-Middle Aged, pubmed-meshheading:21184584-Nail-Patella Syndrome, pubmed-meshheading:21184584-Odds Ratio, pubmed-meshheading:21184584-Self Report, pubmed-meshheading:21184584-Transcription Factors, pubmed-meshheading:21184584-Young Adult
pubmed:year
2011
pubmed:articleTitle
Increased symptoms of attention deficit hyperactivity disorder and major depressive disorder symptoms in Nail-patella syndrome: potential association with LMX1B loss-of-function.
pubmed:affiliation
Department of Psychiatry, Center for Genetic Disorders of Cognition and Behavior, Kennedy Krieger Institute, Baltimore, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural