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Thursday, May 7, 2009
Northwest Hall (Chicago Hilton)
12:00 PM
Background: Clathrin is a protein that is the major constituent of the “coat” of clathrin-coated pits and coated vesicles that are formed during endocytosis of materials at the surface of cells. Clathrin proteins have been implicated in synaptic plasticity. Clathrin assembly protein 3 (AP-3), which is a neuron-specific component of clathrin coated vesicles has been suggested to play a regulatory role in synaptic vesicle recycling since it promotes the assembly of uniform clathrin cages. Scientists have long hypothesized that impairing normal synaptic plasticity might lead to schizophrenia or autism. Very recently a study reported that microRNAs are differentially expressed in autism as compared with age-matched controls and suggested that these microRNAs are very important in regulating synaptic plasticity.
Objectives: The aim of this study is to examine whether clathrin is involved in the pathogenesis of autism by determining the expression levels of clathrin in the brain of autistic individuals and the age-matched controls
Methods: Frozen human brain tissue (frontal cerebral cortex) of autistic patients and age matched control subjects were obtained from the NICHD Brain and Tissue Bank for Developmental Disorders. Donors with autism fit the diagnostic criteria of the Diagnostic and Statistical Manual-IV, as confirmed by the Autism Diagnostic Interview-Revised. Participants were excluded from the study if they had a diagnosis of fragile X syndrome, epileptic seizures, obsessive–compulsive disorder, affective disorders, or any additional psychiatric or neurological diagnoses. This study was approved by the Institutional Review Board of the NY State Institute of Basic Research. In this study, Western Blot Analyses were used to detect the expression levels of clathrin in the brain homogenates.
Results: Our studies show that clathrin is significantly reduced in the brain of autistic children in comparison with age matched controls.
Conclusions: The result from our studies suggests that clathrin may be involved in the pathogenesis of autism by impairing normal synaptic plasticity.
Objectives: The aim of this study is to examine whether clathrin is involved in the pathogenesis of autism by determining the expression levels of clathrin in the brain of autistic individuals and the age-matched controls
Methods: Frozen human brain tissue (frontal cerebral cortex) of autistic patients and age matched control subjects were obtained from the NICHD Brain and Tissue Bank for Developmental Disorders. Donors with autism fit the diagnostic criteria of the Diagnostic and Statistical Manual-IV, as confirmed by the Autism Diagnostic Interview-Revised. Participants were excluded from the study if they had a diagnosis of fragile X syndrome, epileptic seizures, obsessive–compulsive disorder, affective disorders, or any additional psychiatric or neurological diagnoses. This study was approved by the Institutional Review Board of the NY State Institute of Basic Research. In this study, Western Blot Analyses were used to detect the expression levels of clathrin in the brain homogenates.
Results: Our studies show that clathrin is significantly reduced in the brain of autistic children in comparison with age matched controls.
Conclusions: The result from our studies suggests that clathrin may be involved in the pathogenesis of autism by impairing normal synaptic plasticity.