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Autism is a pervasive developmental
disorder (PDD) characterized by abnormalities in social interaction,
communication and behavior (repetitive / perseverative behaviors). The cause is
unknown and treatments limited, but there is no doubt that the origin is
prenatal; children are born with autism even if the symptoms do not appear
clearly enough to diagnose it until eye contact, locomotion and language begin
to emerge. Our lab is working to better understand the causes of this disorder
now estimated by the CDC to occur in 1 out of every 88 births.
Susceptibility genes have also been
associated with autism. One of these is PTEN, which has multiple functions,
including its actions as lipid and protein phosphatases that, through
dephosphorylation, act as a tumor suppressor and negative growth regulator.
PTEN mutations are associated with cell growth and tumorigenesis, and in the
brain have been associated with autism. In collaboration with Steve Danzer, PhD,
who has developed a PTEN brain-specific mutant mouse, we will be investigating
this as a new model of autism-associated behavioral dysfunction.
Two recent epidemiological studies
have shown a significant (doubling to tripling) incidence of Autism Spectrum
Disorder (ASD) in children born to women who took antidepressants during
pregnancy. One of these studies found
that the largest fraction of the risk was from selective serotonin reuptake
inhibitors (SSRIs), the largest group of antidepressants in current use. Unfortunately, studies of this type cannot determine
which antidepressant(s) may be causing ASD (if any) or if non-SSRI
antidepressants are or are not similarly associated with increased ASR
risk. Nor can the human studies
determine the molecular mechanisms of how antidepressants alter the developing
brain to crease the risk of ASD.
Therefore, we testing the effects of two SSRI and one non-SSRI
antidepressant given throughout early brain development in laboratory rats
(from implanation to the end of major neurogenesis (which occurs postnatally in
the rat but prenatally in humans)) to assess how the drugs affect brain
development, neurotransmitters, receptors, and ASD-like behavior. Not only do we wish to determine how
antidepressants may lead to ASD-associated changes, but if different types of
antidepressants carry different risks for inducing ASD-related changes in the
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