Microglial Activation in Adults with Autism Spectrum Disorders

Saturday, May 19, 2012: 10:45 AM
Grand Ballroom East (Sheraton Centre Toronto)
10:15 AM
K. Nakamura1, K. Suzuki2, Y. Ouchi3, M. Tsujii4, G. Sugihara2, Y. Iwata1, K. Matsumoto2, K. Takebayashi2, T. Wakuda1, T. Sugiyama5, Y. Yoshihara1 and N. Mori1, (1)Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Japan, (2)Research Center for Child Mental Development, Hamamatsu University School of Medicine, Hamamatsu, Japan, (3)Molecular Imaging Frontier Research Center, Hamamatsu University School of Medicine, Hamamatsu, Japan, (4)Department of Contemporary Sociology, Chukyo University, Nagoya, Japan, (5)Child and Adolescent Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan
Background:   A growing body of evidence suggests that aberrant immunological systems underlie the pathophysiology of autism spectrum disorders (ASD). However, it is unclear whether immunological alterations, such as excessive microglial activation, are embryonic origin and ongoing mechanism of subjects with ASD.

Objectives: To examine whether microglial activation is increased in individuals with ASD, and whether characteristics of anatomical distribution of the increased, if any, activation of microglia in the brain are different between ASD and controls. 

Methods: Twenty adult males with ASD (age range, 18-31 years; mean [SD] IQ, 93.7 [19.0]) and 20 age- and IQ-matched healthy males as control. Diagnosis of ASD was made by the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview-Revised. Positron emission tomography using a radiotracer [11C](R)-PK11195 was undertaken in each participants. Regional brain [11C](R)-PK11195 binding potential (BP) was estimated by simplified reference tissue model and regarded as a representative measure of microglial activation. 

Results: [11C](R)-PK11195 BP was significantly higher in multiple brain regions in adults with ASD as compared to controls (P < .05, corrected). The brain regions with increased binding potentials included the cerebellum, midbrain, pons, superior temporal and fusiform gyri, and anterior cingulate and orbitofrontal cortices. The most prominent increase was observed in the cerebellum and brainstem. The regional patterns of activated microglia in the different brain areas are regarded to be essentially similar between ASD and control groups. 

Conclusions: Excessive microglial activation was present in multiple brain regions in ASD, especially in the cerebellum and brainstem. The similar parallelism of the pattern of distribution of activated microglia in both ASD and control groups suggest that activated microglia in ASD, as those in controls, are embryonic or fatal origin. 

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