Journal
MOLECULAR PSYCHIATRY
Volume 26, Issue 5, Pages 1659-1669Publisher
SPRINGERNATURE
DOI: 10.1038/s41380-020-0682-z
Keywords
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Funding
- Robert E. and Donna Landreth Fund for the Study of Neuroimmune Interactions in Autism
- Autism Speaks [9258]
- [R01 NS094306-01A1]
- [R01 NS095937-01A1]
- [R01 DA047088-01]
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Lower regional TSPO expression in individuals with ASD compared to controls suggests abnormalities in neuroimmune processes or mitochondrial dysfunction. The stability and replicability of TSPO expression over time in ASD individuals were confirmed by voxelwise analysis.
Mechanisms of neuroimmune and mitochondrial dysfunction have been repeatedly implicated in autism spectrum disorder (ASD). To examine these mechanisms in ASD individuals, we measured the in vivo expression of the 18 kDa translocator protein (TSPO), an activated glial marker expressed on mitochondrial membranes. Participants underwent scanning on a simultaneous magnetic resonance-positron emission tomography (MR-PET) scanner with the second-generation TSPO radiotracer [C-11]PBR28. By comparing TSPO in 15 young adult males with ASD with 18 age- and sex-matched controls, we showed that individuals with ASD exhibited lower regional TSPO expression in several brain regions, including the bilateral insular cortex, bilateral precuneus/posterior cingulate cortex, and bilateral temporal, angular, and supramarginal gyri, which have previously been implicated in autism in functional MR imaging studies. No brain region exhibited higher regional TSPO expression in the ASD group compared with the control group. A subset of participants underwent a second MR-PET scan after a median interscan interval of 3.6 months, and we determined that TSPO expression over this period of time was stable and replicable. Furthermore, voxelwise analysis confirmed lower regional TSPO expression in ASD at this later time point. Lower TSPO expression in ASD could reflect abnormalities in neuroimmune processes or mitochondrial dysfunction.
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