ArticleNature neuroscience2026
Spatiotemporal AI-based modeling of gene regulation and variant effects in the developing human brain using Seal.
Article in Nature neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Understanding how genetic variation shapes gene regulation in the developing human brain remains a central challenge in neuroscience, particularly in transient cell types and developmental stages where data are limited. We present Seal, an interpretable artificial intelligence (AI) transfer learning framework for genome-based modeling of gene expression and variant effects with spatiotemporal resolution across 26 regions, 30 cell types and 7 developmental stages. Seal predictions provide mechanistic interpretation by linking variants to transcriptional regulators in a spatiotemporal context. Applying Seal to genome-wide association studies, we identify shared and distinct regulatory architectures across six neuropsychiatric conditions that align with clinical trajectories. In the Simons Simplex Collection autism cohort whole-genome data, Seal uncovers a significant burden of de novo regulatory variants in transient fetal excitatory neurons, revealing cell-type-specific and stage-specific effects. By connecting genetic variation to spatiotemporal regulatory programs, Seal offers a general framework for uncovering mechanisms of human brain development and disease.
Identifiers
42881222What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.