Editing Openai/69177fbb-14c4-800f-bc57-ccb5a1d88c95 (section)

===== 1. Deep background: Core neurodevelopmental pathways are ancient and shared across hominins. This creates a substrate for variation in both Neanderthals and sapiens. =====
# Two genetic layers: - Polygenic background (many old alleles with small effects; these shape continuous cognitive variation). - Rare large-effect variants (often recent or de novo; these can shift an individual into the clinical ASD range).
# Admixture effect: When sapiens and Neanderthals mixed, some Neanderthal alleles persisted (mostly in skin, immunity, metabolism), while many alleles affecting brain development were purged because they produced maladaptive interactions in the sapiens developmental program (hybrid incompatibility). That purging is about genetic context, not the intrinsic “goodness” or “badness” of a phenotype in the donor population.
# Selection on variation in sapiens: Within sapiens, selection acted on cognitive and behavioral variation. Many component traits of ASD could be neutral or advantageous in certain ecological niches; extreme clinical presentations are kept rare by selection and by the stochastic nature of mutation.
# Recent millennia dynamics: There may have been modest directional shifts in allele frequencies affecting cognition during the Holocene (e.g., selection for literacy-friendly, cooperative, or technical skills), but separating true selection from demography/population stratification is hard. Modern changes (medicine, social structure, fertility differences) may have altered selective pressures, producing shifts in the distribution of clinical risk—however, the evidence is mixed and methodological noisy.