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Openai/69177fbb-14c4-800f-bc57-ccb5a1d88c95
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===== - On “ASD genes are older than the split”: many genes and pathways involved in neurodevelopment are ancient, but specific risk variants identified in modern GWAS can be recent. Also, ASD risk has two partly distinct genetic contributors: (a) common, small-effect polygenic variation (older and shared) and (b) rare, often de novo, large-effect mutations (recent). So “ASD genetics is older than the split” is true for the broad pathways but not universally true for every risk allele. ===== * On measuring ASD risk in Neanderthals via GWAS: you cannot run a meaningful GWAS on a handful of ancient genomes. GWAS requires large samples and the same population structure. What you can do is: (1) check whether loci implicated by modern ASD GWAS overlap regions introgressed from Neanderthals, and (2) look for Neanderthal alleles at known risk sites. Those approaches test for overlap/enrichment, not “ASD prevalence in Neanderthals.” * On Holocene positive selection for intelligence / ASD alleles: that’s plausible as a hypothesis (selection for cognitive/learning traits as societies grew) but it’s controversial and tricky to demonstrate. Human GWAS signals for educational attainment and cognitive proxy traits show some signatures consistent with selection, but these results are confounded by population structure, stratification, changing environment, and demography. Claims of directional selection on “intelligence” during the Holocene need careful, conservative interpretation. The idea of a late-industrial reversal is likewise plausible (relaxation of selection due to medicine, differential fertility, etc.), but again empirical support is mixed and contested.
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