Brandon J. Vaglio

ORCID: 0000-0002-2016-9212
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About
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Research Areas
  • RNA and protein synthesis mechanisms
  • Infectious Encephalopathies and Encephalitis
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Congenital heart defects research
  • RNA Research and Splicing
  • EEG and Brain-Computer Interfaces
  • Neuroscience and Neural Engineering
  • Single-cell and spatial transcriptomics
  • Tryptophan and brain disorders
  • interferon and immune responses
  • Neural dynamics and brain function

Rutgers, The State University of New Jersey
2023-2025

Rutgers Sexual and Reproductive Health and Rights
2024

Summary While recent work has identified roles for immune mediators in the regulation of neural activity, capacity cell intrinsic innate signaling within neurons to influence neurotransmission remains poorly understood. However, existing evidence linking with neuronal function suggests that modulation may serve previously undefined host protection during infection central nervous system. Here, we identify a specialized RIPK3, kinase traditionally associated necroptotic death, preserving...

10.1101/2024.04.26.591333 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-04-28

The 1.6-megabase deletion at chromosome 3q29 (3q29Del) is the strongest identified genetic risk factor for schizophrenia, but effects of this variant on neurodevelopment are not well understood. We interrogated developing neural transcriptome in two experimental model systems with complementary advantages: isogenic human cortical organoids and isocortex from 3q29Del mouse model. profiled transcriptomes that were aged 2 12 months, as perinatal isocortex, all single-cell resolution. Systematic...

10.1126/sciadv.adh0558 article EN cc-by-nc Science Advances 2023-08-16

Recent advances in the genetics of schizophrenia (SCZ) have identified rare variants that confer high disease risk, including a 1.6 Mb deletion at chromosome 3q29 with staggeringly large effect size (O.R. > 40). Understanding impact (3q29Del) on developing CNS may therefore lead to insights about pathobiology schizophrenia. To gain clues molecular and cellular perturbations caused by deletion, we interrogated transcriptomic effects two experimental model systems complementary advantages:...

10.1101/2023.01.27.525748 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-01-28
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