Our SNP-h2 and genetic correlation findings confirm that neurological disorders are genetically distinct from one another and from psychiatric disorders and SUDs, as well as from behavioral/quantitative phenotypes, which is in line with previous evidence [3, 10]. Consistent with these findings, we found that GWAS findings from psychiatric disorders, SUDs, and brain-related behavioral/quantitative phenotypes, but not neurological disorders, consistently map to excitatory hippocampal pyramidal neurons (CA1), excitatory pyramidal neurons (SS) and inhibitory MSNs, and much less to glial and embryonic cells. This concurs with previous lines of evidence pointing to neurological disorders being genetically and functionally distinct from psychiatric disorders, SUDs, and brain-related behavioral/quantitative phenotypes [3, 10]. Alzheimer’s disease was the only malady targeted here that showed evidence of exclusively human glial cells being implicated, underscoring the importance of key transcriptomic differences between human and mouse microglial signatures [33]. We confirmed our main findings with multiple external scRNA datasets using FUMA. This provides further evidence that genetic underpinnings of neurological disorders are distinct from those of psychiatric, SUDs, and behavioral/quantitative phenotypes [8, 10]. Our main findings were based on the
