2007 Fiscal Year Final Research Report Summary
The study related to the neurophysical mechanism of high-functioning autism for using the method of neuroimaging and molecular biology
| Project/Area Number |
18390321
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
NAKAMURA Kazuhiko Hamamatsu University School of Medicine, The medical department, Senior Assistant Professor (80263911)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Norio Hamamatsu University School of Medicine, The medical department, Professor (00174376)
OUCHI Yasuomi Hamamatsu University School of Medicine, Visiting Professor (40436978)
TUJII Masatsugu Hamamatsu University School of Medicine, Visiting Professor (20257546)
TAKEI Noriyoshi Hamamatsu University School of Medicine, Research Center for Child Mental Development United Graduate School of Child Development, Professor (80206937)
MINABE Yoshio Hamamatsu University School of Medicine, Kanazawa University Hospital, Professor (60181947)
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| Project Period (FY) |
2006 – 2007
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| Keywords | autism / neuroimaging / gene |
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| Research Abstract |
To determine the occurrence of changes in the binding of serotonin and dopamine transporters, which are highly selective markers for their respective neuronal systems. Using positron emission tomography, we measured the binding of brain serotonin and dopamine transporters in each individual with the radioligands carbon [11C]McN-5652 and [11C]WIN-35,428, respectively. Participants recruited from the community. Twenty men (age range, 18-26 years ; mean [SD] IQ, 99.3 [18.1]) with autism and 20 age- and IQ matched control subjects. Serotonin transporter binding was significantly lower throughout the brain in autistic individuals compared with controls (P_.05, corrected). Specifically, the reduction in the anterior and posterior cingulated cortices was associated with the impairment of social cognition in the autistic subjects (P_.05, corrected). A significant correlation was also found between repetitive and/or obsessive behavior and interests and the reduction of serotonin transporter binding in the thalamus (P_.05, corrected). In contrast, the dopamine transporter binding was significantly higher in the orbitofrontal cortex of the autistic group (P_.05, corrected in voxelwise analysis). In the orbitofrontal cortex, the dopamine transporter binding was significantly inversely correlated with serotonin transporter binding (r=-0.61 ; P=.004). The brains of autistic individuals have abnormalities in both serotonin transporter and dopamine transporter binding. The present findings indicate that the gross abnormalities in these neurotransmitter systems may underpin the neurophysiologic mechanism of autism.
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