It’s multiple conditions we group together naively based on surface level symptoms. Same for many disorders.
The type that comes with gender and sexual fluidity, bendyness, ADHD = rccx caused ASD.
Then that will have multiple subtypes based on mutation combination within the rccx module.
(The RCCX module would’ve been excluded from the genetic analysis the report this article is based on - due to its complexity).
Severe/non-verbal ASD is more likely completely unrelated and caused by dendritic abnormalities (reduced or excessive branching, immature spines, disrupted morphology, etc)
You seem to have a more in depth grasp of the precise genetics involved here than I do, what would your opinion be of Dr. Frye’s concept of “Cerebral Folate Disorder” that I mention in another comment?
Here’s a paper from him and his team, he has many though:
As best I can tell, he is focused on the non-syndromic, non-verbal, uh, what this recent paper OP is about seems to categorize as ‘early diagnosis autism’.
He’s got a cluster of specific mutations that produce an evidenced, differing neurochemistry in the brain, and apparently a potential treatment for that ‘subypr/component’ as well?
I… don’t agree with his general description of autism as basically only the kind that makes you developmentally delayed, but, if you can get past that… do you think he may be onto something as far as that being an distinct ‘type’ of autism?
Also, apologies if I am using some terms incorrectly or innacurately, I am not a neuroscientist.
It’s multiple conditions we group together naively based on surface level symptoms. Same for many disorders.
The type that comes with gender and sexual fluidity, bendyness, ADHD = rccx caused ASD.
Then that will have multiple subtypes based on mutation combination within the rccx module.
(The RCCX module would’ve been excluded from the genetic analysis the report this article is based on - due to its complexity).
Severe/non-verbal ASD is more likely completely unrelated and caused by dendritic abnormalities (reduced or excessive branching, immature spines, disrupted morphology, etc)
You seem to have a more in depth grasp of the precise genetics involved here than I do, what would your opinion be of Dr. Frye’s concept of “Cerebral Folate Disorder” that I mention in another comment?
Here’s a paper from him and his team, he has many though:
https://pmc.ncbi.nlm.nih.gov/articles/PMC5794882/
As best I can tell, he is focused on the non-syndromic, non-verbal, uh, what this recent paper OP is about seems to categorize as ‘early diagnosis autism’.
He’s got a cluster of specific mutations that produce an evidenced, differing neurochemistry in the brain, and apparently a potential treatment for that ‘subypr/component’ as well?
I… don’t agree with his general description of autism as basically only the kind that makes you developmentally delayed, but, if you can get past that… do you think he may be onto something as far as that being an distinct ‘type’ of autism?
Also, apologies if I am using some terms incorrectly or innacurately, I am not a neuroscientist.