There are perverse consequences in brain chemistry and signalling: flooding a brain deficient in glutamate processing receptors with glutamate may not help, it may overload pathways and cause hindrance, not compensation.

Signs like this may be consequential, or related but not causal, or may simply turn out to be wrong.

IF a small sample effect turns out to be indicative of a larger property, and IF it's shown to be causal and IF remeditation involves boosting blood borne glutamate or precursors is 3 stacked IF.

IF its detectable in a young brain it could be diagnostic.

IF its detectable in a young brain and amenable to gene therapy and IF it's causative then treatment would be useful.

IF excess glutamate is not a problem and dietary supplemented sources cross the blood brain barrier and don't trip over homeostasis then it's possibly worth exploring.

(Not a scientist, not a biologist)

This is more or less not true. If it doesn't hinder a person in any aspect of their life, they don't fit the DSM-V criteria for a diagnosis.

(Many neurodivergent people aren't hindered by autism because they have some other neurodivergence, but that's a different issue with this sentence)

Neurons specifically increase / decrease receptor density in response to environmental factors, eg: use of SSRI's. Any excess of neurotransmitter would likely lead to reduction in receptor density as part of the response. So the story can be as much about an excess of neurotransmitter as it is about depletion of the receptor.

Perhaps the main story here is they can use EEGs as a proxy for measuring this effect so they don't need to put people through PET scans to do wider studies.

> We want to start creating a developmental story and start understanding whether the things that we’re seeing are the root of autism or a neurological consequence of having had autism your whole life

But here there’s a basic design flaw. This is a study of 16 ASD cases and 16 neurotypical controls. Small sample sizes like this require careful matching. The problem: the autistic subjects are 100% White but controls are 37.5% White. That imbalance can’t be waved away with statistics or Jedi mind tricks. Recruiting matched neurotypicals would have been straightforward.

One other issue is high heterogeneity within the two groups. In their Figure 1 (sorry behind a paywall), 4 - 6 of the autistic individuals have low mGlu5 levels across all regions. Two or three neurotypicals have high levels. Are these distributions actually normal, or are subgroups driving effects? It would help to know whether the participants’ GRM5 genotypes were informative wrt these subgroups. They weren’t checked.

[1] "The findings support the idea that an imbalance of excitatory and inhibitory signals in the brain could be contributing to traits associated with autism, the researchers say." https://medicine.yale.edu/news-article/molecular-difference-...

[2] "Converging evidence from diverse studies suggests that atypical brain connectivity in autism affects in distinct ways short- and long-range cortical pathways, disrupting neural communication and the balance of excitation and inhibition." https://doi.org/10.3389/fnhum.2013.00609

I don't know much about the biochemistry here, I assume this is not something like GABA that can be directly supplemented. But maybe there are precursor nutritional and supplemental substances that can help these people upregulate how much of the glutamate molecule in question the body can produce.

So we might be able to make all the non-autistic people autistic? What would the world be like if everyone was mildly autistic?

It's somewhat comparable to using a handheld magnifying glass on petri dishes and making broad claims about virus morphology. EEG is great, but I'm not sure I buy the methodology in this case. You need a huge N and much better experimental design and absolutely zero hype unless or until you show results with scientific rigor.

This sort of clickbait almost makes me view this type of research as a flavor of pseudo-science. The framing is misleading at best, but the full throated embrace of the clickbait and hype machine is awful.

It's funding bait, narrative manipulation, etc, and it'll either be part of something replicated and justified with much better experiments, or it'll just fade away into oblivion, with no repercussions for any involved should the outcome not actually benefit anyone or anything. There's not even a negative incentive, mGlu5 and "imbalance" claims have been made for decades, and they keep circling the questions but don't ever seem to actually "do" real science.

Shows how shockingly unaware even researchers are on how broad and nonspecific the diagnosis of autism is...

Were these 16 people hypo or hyper sensitive? Which of their five senses were involved? All? Some? Were some senses hyper and others hypo?

Need to start with categorization and specificity before we can make meaningful progress in research

As an example: I'm autistic and I learn inside-out, building larger new concepts out of smaller existing ones; those with Asperger's on the other paw, learn outside-in instead, breaking down larger existing concepts into smaller new ones; both are part of the "autism spectrum", but differ very fundamentally.

Given that the origin of "autism" is simply "thinking that differs from usual", there's no evidence that there is a single underlying cause to find, nor that generalizations across the entire spectrum will reveal much of anything other than coincidence.

I believe we need to individualize new research to the variants that we now know exist, because otherwise we will continue to all-but erase anything that isn't common to the entire spectrum.

[0]: https://www.medrxiv.org/content/10.1101/2024.08.15.24312078v...