The metabotropic glutamate receptor subtype 5 (mGlu5) is involved in the central mechanism of action of paracetamol (acetaminophen), where the bioactive metabolite AM404 activates the TRPV1 channel–mGlu5 receptor–PLC–DAGL–CB1 receptor signaling cascade in the periaqueductal grey, contributing to its analgesic effect.
> 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
Yeah, how many studies are done a year? Random chance is the #1 explanation with that small of a sample size. It doesn't take a degree in stats say that the next thing that needs to be done is to replicate the study a few times before making any claims or searching for any publicity. This subject is so emotional for the families involved that publicizing without more confirmation is a bit irresponsible especially if it is easy to do follow-up studies.
Interesting indeed. Does such a finding suggest any worthwhile easy-to-try 'treatments' that may help alleviate symptoms?
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.
Unless you can get the blastocyst and fetus to take supplements, any treatment would be attempting to undo the effects that have already taken place.
For now, your best options are ESDM, occupational therapy, modified CBT, ABA, or neurofeedback, depending on your circumstances and presentation. Except for neurofeedback, these are behavioral approaches, so the architectural and neural activity variations aren't directly addressed.
> 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.
Reduce receptors. This might suggest a _developmental_ or genetic link. Think of this more like "height" or a particular "facial feature" of a person.
There isn't enough information to start doing that. Consider: UV exposure results in sunburn, cellular damage, and increased skin pigmentation. We have medication that reduces skin pigmentation. Should we give it to people who experience chronic sunburn?
> 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
Wish I could read the paper.
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.
For now, your best options are ESDM, occupational therapy, modified CBT, ABA, or neurofeedback, depending on your circumstances and presentation. Except for neurofeedback, these are behavioral approaches, so the architectural and neural activity variations aren't directly addressed.
> 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.
Reduce receptors. This might suggest a _developmental_ or genetic link. Think of this more like "height" or a particular "facial feature" of a person.