TL;DR

Researchers at Yale used MRI, PET and EEG to compare 16 autistic adults with 16 neurotypical controls and found reduced availability of the metabotropic glutamate receptor 5 (mGlu5) across autistic brains. The result supports hypotheses about excitatory/inhibitory signaling imbalance and may inform future diagnostics and interventions.

What happened

A Yale School of Medicine team published a study in The American Journal of Psychiatry comparing brain scans from 16 autistic adults and 16 neurotypical participants. Investigators combined magnetic resonance imaging for anatomy and positron emission tomography to map molecular-level glutamate receptor availability; PET results showed lower brain-wide availability of metabotropic glutamate receptor 5 (mGlu5) in the autistic group. Fifteen autistic participants also had electroencephalogram recordings, and the researchers report correlations between those EEG measures and lower mGlu5 levels. The authors frame the finding in terms of an excitatory–inhibitory signaling balance in the brain and note PET’s cost and radiation exposure as limitations. The study included autistic adults with average or above-average cognitive ability; the team is developing lower-radiation PET methods to enable studies in children and groups not represented here. Whether the receptor difference is causal or a long-term consequence remains unresolved.

Why it matters

  • Identifies a measurable molecular difference linked to glutamate signaling in autistic adult brains, moving beyond symptom-based diagnosis.
  • Supports the excitatory/inhibitory imbalance hypothesis that aims to explain diverse features of autism.
  • Points to mGlu5 as a potential biological target for future research into diagnostics or treatments.
  • Suggests EEG, a cheaper and more accessible tool, could help probe excitatory function when PET is impractical.

Key facts

  • Study published in The American Journal of Psychiatry.
  • Participants: 16 autistic adults and 16 neurotypical controls.
  • Main finding: reduced availability of metabotropic glutamate receptor 5 (mGlu5) across autistic participants’ brains.
  • Imaging methods: MRI for anatomy and PET to assess molecular receptor availability.
  • Fifteen autistic participants underwent EEG; those electrical measures were associated with lower mGlu5 availability.
  • All autistic participants had average or above-average cognitive abilities.
  • Researchers noted PET is costly and involves radiation exposure, motivating interest in EEG as a complementary tool.
  • Investigators include James McPartland, David Matuskey, Adam Naples and Richard Carson from Yale School of Medicine.

What to watch next

  • Whether lower mGlu5 availability is a cause of autism or a consequence of long-term neurodevelopmental differences — not confirmed in the source.
  • Planned studies using lower-radiation PET techniques to include children and adolescents (confirmed in the source).
  • Efforts to develop or test interventions that target mGlu5 as a therapeutic approach — not confirmed in the source.
  • Validation of EEG measures as a practical proxy for excitatory glutamate function in larger and more diverse samples (confirmed in the source).

Quick glossary

  • mGlu5 (metabotropic glutamate receptor 5): A subtype of glutamate receptor involved in modulating neuronal signaling and synaptic activity.
  • Glutamate: The brain’s most common excitatory neurotransmitter, which promotes neural firing and communication.
  • Positron Emission Tomography (PET): A molecular imaging technique that uses radioactive tracers to visualize biological processes in the body.
  • Electroencephalogram (EEG): A noninvasive method that records electrical activity from the scalp to assess brain function.
  • Excitatory/inhibitory balance: The equilibrium between neural signals that promote activity (excitatory) and those that suppress it (inhibitory), important for normal brain function.

Reader FAQ

What did the study find?
Researchers observed reduced availability of the mGlu5 glutamate receptor across the brains of autistic adults compared with neurotypical controls.

Who was included in the research sample?
The study compared 16 autistic adults (all with average or above-average cognitive abilities) and 16 neurotypical adults; 15 autistic participants also had EEG recordings.

Does this mean there’s a new treatment for autism now?
No. The source states there are currently no medications that treat the core difficulties of autism; the findings may guide future research into targets but do not represent an existing therapy.

Will EEG replace PET for this kind of research?
Not according to the authors: EEG may provide a cheaper, more accessible way to probe excitatory function, but it is not expected to fully replace PET scans.

Is it clear whether the receptor change causes autism?
Not confirmed in the source.

NEW RESEARCH QUICK READ Researchers Discover Molecular Difference in Autistic Brains By Isabella Backman December 19, 2025 5 Minute Read Share Listen to this article 00:00 06:10 Yale School of…

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