alt Hacker NewsHomeostasis across the blood brain barrier makes me suspect trivial approaches to boosting glutamate won't work. But this even begs the question if boosting available glutamate would be the right thing.
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)
It seems you are assuming that because the majority of people have a certain quantity of glutamate receptors, that they are the healthy ones and that we should be trying to bring autistic people up to that level. Is that right?
Why not consider the opposite, that the most beneficial quantity of glutamate receptors could be somewhere below the typical amount? If that were true, then we could try to help others reduce their glutamate receptor level to become healthier and more successful (and a little more autistic).
If we found, say, an association between a lower level of neurological characteristic X and concert-level piano skill, then those who aspire to play that instrument at an elite level might try to decrease X. The fact that most of us are rubbish piano players would not be evidence that lower levels of X are harmful, but very much the opposite.