Alessandro Vitriolo

The paper maps RNA-DNA interactions in 16 human cell types, showing cell-type-specific and dynamic networks that correlate with gene regulation and disease traits.

The paper maps RNA-chromatin interactions in human prefrontal cortex, revealing co-regulatory changes linked to brain evolution and disease pathways.

This paper establishes a defined feeder-free system to convert human PGC-like cells to pluripotent stem cells, tracking transcriptional and epigenomic transitions using multi-omic analysis.

The paper longitudinally profiles cerebellar organoids, benchmarks them against fetal data, and models mutations linked to autism and human brain evolution.

The paper uses combinatorial CRISPR-Cas9 perturbations in brain organoids to uncover regulatory hierarchies of human-specific genes involved in cortical evolution.

This study identifies the ADNP-KDM1A-GTF2I complex as critical for neural differentiation balance in HVDAS by repressing transposable elements and regulating gene transcription.

This study investigates how YY1 mutations disrupt corticogenesis by altering transcriptional networks in neural progenitors and neurons, with non-cell-autonomous effects on astrocytes.

This study identifies a human-specific CHD2 regulatory variant that influences cortical development tempo via lysosomal homeostasis, showing therapeutic potential through lysosomal restoration.

The paper develops and validates multiplexing strategies for brain organoids combined with single cell RNA-seq to study neurodevelopmental trajectories across multiple genetic lines.

The paper curates causal gene-protein interactions linked to autism and develops tools to explore their functional relationships with phenotypes and pathways.

This study investigates how 7q11.23 CNVs affect protein synthesis and neuronal excitability in neurodevelopmental disorders using patient-derived neurons and multi-omics approaches.

The paper quantifies ADNP mutation mosaicism across tissues in a post-mortem autistic individual, showing post-zygotic, tissue-specific mutation patterns and ruling out environmental factors.

This study investigates how KMT2D mutations in Kabuki Syndrome disrupt neuronal function through chromatin and transcriptional changes, independent of H3K4me1.