Found 'Clue' That Can Fundamentally Treat Autism Spectrum Disorder

Looking at the original paper the following is evident, Changes to genes expressing "Contactin-associated protein-like 2 (CNTNAP2) can cause many neurological disabilities in humans, including ASD and intellectual disability." They are looking at a subset of autistics, those with 'CNTNAP2-associated ASD'. They have produced 'knock out' mouse models for  'CNTNAP2-associated ASD', and these mice behave in 'asocial' ways - so they are claimed to mirror autism in humans. They have compared the molecular basis of the metabolic functioning of their mice brains - using mass spectrometry-based proteometabolomics - with expression from human brain organoids from autistic people and found similarities. The paper ends with, "These genes should be further studied within ASD models to determine whether they are central to ASD models and patients." 

OK, the take-home message is that this is probably not relevant for the majority of autistic people, just those with a specific, and genetically 'simple', form of autism 'CNTNAP2-associated ASD'. The paper does not seem to give any information about how prevalent CNTNAP2-associated ASD is in the overall autistic population. It does not come close to suggesting a 'cure for ASD'.

Looking at the original paper the following is evident, Changes to genes expressing "Contactin-associated protein-like 2 (CNTNAP2) can cause many neurological disabilities in humans, including ASD and intellectual disability." They are looking at a subset of autistics, those with 'CNTNAP2-associated ASD'. They have produced 'knock out' mouse models for  'CNTNAP2-associated ASD', and these mice behave in 'asocial' ways - so they are claimed to mirror autism in humans. They have compared the molecular basis of the metabolic functioning of their mice brains - using mass spectrometry-based proteometabolomics - with expression from human brain organoids from autistic people and found similarities. The paper ends with, "These genes should be further studied within ASD models to determine whether they are central to ASD models and patients." 

OK, the take-home message is that this is probably not relevant for the majority of autistic people, just those with a specific, and genetically 'simple', form of autism 'CNTNAP2-associated ASD'. The paper does not seem to give any information about how prevalent CNTNAP2-associated ASD is in the overall autistic population. It does not come close to suggesting a 'cure for ASD'.