Genome-wide association studies have generated an increasing number of common genetic
variants associated with neurological and psychiatric disease risk. An improved under-
standing of the genetic control of gene expression in human brain is vital considering this is
the likely modus operandum for many causal variants. However, human brain sampling
complexities limit the explanatory power of brain-related expression quantitative trait loci
(eQTL) and allele-specific expression (ASE) signals. We address this, using paired genomic
and transcriptomic data from putamen and substantia nigra from 117 human brains, inter-
rogating regulation at different RNA processing stages and uncovering novel transcripts. We
identify disease-relevant regulatory loci, find that splicing eQTLs are enriched for regulatory
information of neuron-specific genes, that ASEs provide cell-specific regulatory information
with evidence for cellular specificity, and that incomplete annotation of the brain tran-
scriptome limits interpretation of risk loci for neuropsychiatric disease. This resource of
regulatory data is accessible through our web server, http://braineacv2.inf.um.es/