Summary: A recent study used PET imaging to examine synaptic connections in autistic and non-autistic adults, marking the first time this technology was applied to autism research. Findings show autistic adults have fewer synapses, or connections between brain cells, which closely relates to social and communicative differences in autism.
The study indicates that lower synaptic density may underlie some of the challenges in social interaction and communication experienced by autistic individuals. Researchers believe these insights could guide future support and interventions for autism. This research highlights a potential physiological basis for social differences in autism.
Key Facts
- PET imaging shows fewer brain synapses in autistic adults compared to non-autistic adults.
- Fewer synapses strongly correlate with social and communicative challenges in autism.
- This insight may shape better-targeted support strategies for autistic individuals.
Source: Yale
New research published in Molecular Psychiatry looks at the differences in social interaction and communication observed in autistic and non-autistic adults, using positron emission tomography (PET), a type of brain imaging.
In the study, PET was used to directly measure the connections between brain cells (synapses).
“This is the first time it has been done in autism, and we learned that autistic adults have fewer of these synapses throughout their brains. We also learned that this was very strongly related to the social and communicative differences in autism,” says James McPartland, Ph.D., Harris Professor in the Child Study Center at Yale School of Medicine.
In this imaging study, McPartland says they also learned that the fewer synapses a person had, the more likely they were to show difficulties in social interaction and communication.
These findings give insight as to what might be actually happening in the brain that accounts for the challenges many autistic people experience, he says.
“It gives us important ideas about how we might better support autistic people,” says McPartland.
About this autism research news
Author: James McPartland
Source: Yale
Contact: James McPartland – Yale
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“11C-UCB-J PET imaging is consistent with lower synaptic density in autistic adults” by James McPartland et al. Molecular Psychiatry
Abstract
11C-UCB-J PET imaging is consistent with lower synaptic density in autistic adults
The neural bases of autism are poorly understood at the molecular level, but evidence from animal models, genetics, post-mortem studies, and single-gene disorders implicate synaptopathology.
Here, we use positron emission tomography (PET) to assess the density of synapses with synaptic vesicle glycoprotein 2A (SV2A) in autistic adults using 11C-UCB-J.
Twelve autistic (mean (SD) age 25 (4) years; six males), and twenty demographically matched non-autistic individuals (26 (3) years; eleven males) participated in a 11C-UCB-J PET scan. Binding potential, BPND, was the primary outcome measure and computed with the centrum semiovale as the reference region.
Partial volume correction with Iterative Yang was applied to control for possible volumetric differences. Mixed-model statistics were calculated for between-group differences.
Relationships to clinical characteristics were evaluated based on clinician ratings of autistic features. Whole cortex synaptic density was 17% lower in the autism group (p = 0.01). All brain regions in autism had lower 11C-UCB-J BPND compared to non-autistic participants.
This effect was evident in all brain regions implicated in autism. Significant differences were observed across multiple individual regions, including the prefrontal cortex (−15%, p = 0.02), with differences most pronounced in gray matter (p < 0.0001). Synaptic density was significantly associated with clinical measures across the whole cortex (r = 0.67, p = 0.02) and multiple regions (rs = −0.58 to −0.82, ps = 0.05 to <0.01).
The first in vivo investigation of synaptic density in autism with PET reveals pervasive and large-scale lower density in the cortex and across multiple brain areas. Synaptic density also correlated with clinical features, such that a greater number of autistic features were associated with lower synaptic density.
These results indicate that brain-wide synaptic density may represent an as-yet-undiscovered molecular basis for the clinical phenotype of autism and associated pervasive alterations across a diversity of neural processes.
