Im Gehirn autistischer Menschen gibt es weniger spezifische Rezeptoren für Glutamat, den häufigsten erregenden Neurotransmitter im Gehirn. Die verminderte Verfügbarkeit dieser Rezeptoren kann mit verschiedenen Merkmalen im Zusammenhang mit Autismus verbunden sein.
https://medicine.yale.edu/news-article/molecular-difference-in-autistic-brains/
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Yale School of Medicine (YSM) scientists have discovered a molecular difference in the brains of autistic people compared to their neurotypical counterparts.
Autism is a neurodevelopmental condition associated with behavioral differences including difficulties with social interaction, restrictive or intense interests, and repetitive movements or speech. But it’s not clear what makes autistic brains different.
Now, a new study in The American Journal of Psychiatry has found that **brains of autistic people have fewer of a specific kind of receptor for glutamate, the most common excitatory neurotransmitter in the brain. The reduced availability of these receptors may be associated with various characteristics linked to autism.**
While many neurodivergent people aren’t hindered by autism and may not need or want medication, novel treatments could help those on the spectrum that experience symptoms that affect their quality of life.
For those interested, here’s the link to the peer reviewed journal article:
https://psychiatryonline.org/doi/10.1176/appi.ajp.20241084
Oh is this that same research that one autistic girl is always talking about that the ivy League folks stole from her?
The relevant question here is what they considered autistic.
Would appreciate an ELI5 on what effects insufficient glutamate receptors would have on a person if anyone wants to explain!
People are very concerned with autism in recent years. I’m all for progress but I think people should lighten up. Society is static.. but overall pretty solid. It’s not made for everyone.. it’s made to help *the most* people.
So you’re always going to have someone who’s a black sheep. Maybe you plop them into Iceland, they excel?
One last point there.. that diagnosis won’t help you. There’s literally nothing it can help with if you’re high functioning. At best it probably makes you a target in this current world.
I think we should focus more on the inclusivity stuff. Not forcing it, educating people young is important. Part a certain point.. you’ve created an idiot and no amount of knowledge will supplement that.
Are there prior PET or post-mortem studies that reported similar glutamate receptor differences, or is this the first evidence at this scale?
I knew i need more Mono sodium Glutamate
Haven’t podcasters talking about this for years? Is it actually true?
Omg could this be why so many of us have junk food as our save foods?
If that is indeed true and if lack of glutamate is responsible for (some) autistic traits, would glutamate reuptake inhibitors have an effect?
Edit: a cursory search shows increased glutamate levels in some autistic patients. In these cases, inhibitors are probably counterproductive.
Still, I’d love someone with expertise chiming in.
Below is the abstract from the actual paper. This is a very low sample number and would need to be repeated in hundreds if not thousands of patients.
Lower mGluR5 receptors. These are metabotropic type (m in mGluR5). Metabotropic means they signal downstream (intracellularly/internally) via activation of G proteins.
“Abstract
Objective:
Autism spectrum disorder is a prevalent and heterogeneous condition with features ranging from social and communication differences to sensory sensitivities. Differences in excitatory neurotransmission have been identified in autism, but the molecular underpinnings are poorly understood. To investigate the mechanism underlying these observed differences, the authors assessed glutamatergic receptor density in autistic adults using positron emission tomography (PET) and related it to a functional EEG measure of excitatory activity.
Methods:
Metabotropic glutamate receptor 5 (mGlu5) availability was compared in autistic (N=16) and neurotypical (N=16) adults between 18 and 36 years of age, using the PET tracer 3-[18F]fluoro-5-(2-pyridinylethynyl) benzonitrile ([18F]FPEB). The PET outcome measure was volume of distribution (VT) computed with equilibrium analysis using a venous input function and partial volume correction. Group differences were quantified using mixed-model analyses. Heterogeneity was further parsed within the autistic group by quantifying the relationship between receptor availability and the slope of the EEG power spectrum, an index of excitatory-inhibitory balance. Correlations between EEG and VT were calculated using Spearman’s rho.
Results:
Across all brain regions, mGlu5 availability was significantly lower (by ~15%) in autistic relative to neurotypical control participants. Group differences were generally greatest in the cerebral cortex. Within the autistic group, mGlu5 availability in all regions was significantly correlated with the slope of the EEG (e.g., cerebral cortex, r=0.67), such that shallower slope was associated with lower mGlu5 availability.
Conclusions:
This brain-wide investigation of mGlu5 availability with PET revealed pervasive lower mGlu5 availability across multiple brain areas in autism. Additionally, multimethod analyses revealed associations with a noninvasive electrophysiological index of excitatory neurotransmission. These results indicate that lower brain-wide mGlu5 availability may represent a molecular mechanism underlying altered excitatory neurotransmission that has the potential to stratify the heterogeneous autism phenotype.”