| Co-Investigator(Kenkyū-buntansha) |
MORI Norio Hamamatsu University School of Medicine, Department of Psychiatry and Neurology, Professor (00174376)
TAKEI Noriyoshi Hamamatsu University School of Medicine, Osaka-HamamatsuJoint Resarch Centerfor Child Mental Development, Professor (80206937)
NAKAMURA Kazuhiko Hamamatsu University School of Medicine, Hospital, Lecturer (80263911)
TSUJII Masatsugu Chukyo University, Faculty of Social Science, Professor (20257546)
IWATA Yasuhide Hamamatsu University School of Medicine, Department of Psychiatry and Neurology, Assistant Professor (10285025)
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| Research Abstract |
Background Autism is a neurndevelopmental disorder characterized by poor trial cognition and, by restictod and stereotyped patterns of behavior and interests Evidence suggests that genetic factors play pivotal roles in the aetiology of autistic disorder, whilst. No family history of autistic and Mated disorders can he found in approximately 2 of 3 individuals with autism. On the other hand, nemoimaging studies have suggested that. Structural almonnalities are mnsistently found in brain of individuals with autistic disorder: Tb this point, it remains to be determined whether structuml abnormalities are connected with familial loading to autistic disorder, other-wile, what. Factors, particularly non-genetic litiors (e.g. advanced paternal age at birth), ming for such bruin abnormalities should be expload Objediues We examined 1) whether structural abnormalities rue related to diagnosis of autistic disorder and family history of autistic di: ander and 2) whether such abnormalities me rel
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ated to advanced paternal age at birth. Method Poulton drug-naive male subjects with autistic &senior (mean age 2,1.2 SD 1.1) and 11 healthy male wilutthers (mean age 22.8 SD 1.6) participated in this study. Diagnosis was confirmed using a semi-structured interview, the Autism Di: ann.: tic interview-Revised. Positive family history of autism was defined such that the individual has at least one first-degree relative with lesser variant (of autistic disorder, defined by I'iven, et. Al., 1997)", which was examined through an interview with at least one family member in addition to the participants lb: Mt.: structural abnormalities, we conducted a AIRIsam for each participant. The vosel-wise analyses of images were conducted using statistical pmumetric mapping software (SPM2; hturftwwfilion.uclacads main hi of the measurement were total brain vol tne, total gray matter volume, total white matter volume, left and right hippotnmpal volumes, and total cereballar volume, each of which was standardized using mean value of total brain volume of the control individuals. Results No volume dillerence was found in areas of inkiest between 14 individuals with autisticdisorder and 11 controls. Even alter age WAS adjusted for Among 14 individuals with autistic disorder 5 had the father with lesser variant, whereas no father with hisser variant was found in control group. Thenifine we comparad mean volume of areas of interest among 5 individual with familial autism (having a father with lesser variant), 9 individuals with non-familial autism, 11 control individuals. For left hippommpal volume, individuals with familial autistic disorder indicated the highest mean value (2.76m1), control individuals the Rcond (2.57ml), and the individuals with non-fitmilial autism the lowest (2.36ml), the dillbrence between two groups of autistic disorder being statisticallysignificant Althoughpaternal age wasslightlyhigher in 14 individuals with autism (32.0 yrs) than controls (31.4 yrs), no such difference was found between two groups of autistic disorder. Conslusion Abnormality in left hippocampal volume may be an indicator for familial/non-familial autistic disorder. Less
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