Publications by authors named "G Ciceri"
Disruption of parvalbumin positive (PVALB+) cortical interneurons is implicated in the pathogenesis of schizophrenia. However, how these defects emerge during brain development remains poorly understood. The protracted maturation of these cells during postnatal life has made their derivation from human pluripotent stem cells (hPSCs) extremely difficult, precluding hPSC-based disease modeling of their role in neuropsychiatric disease.
View Article and Find Full Text PDFThe development of functional neurons is a complex orchestration of multiple signaling pathways controlling cell proliferation and differentiation. Because the balance of antioxidants is important for neuronal survival and development, we hypothesized that ferroptosis must be suppressed to gain neurons. We find that removal of antioxidants diminishes neuronal development and laminar organization of cortical organoids, which is fully restored when ferroptosis is inhibited by ferrostatin-1 or when neuronal differentiation occurs in the presence of vitamin A.
View Article and Find Full Text PDFArticle Synopsis
- The study identifies two cases of herpes simplex virus 1 (HSV-1) encephalitis in children linked to rare genetic variants of the TMEFF1 gene, which plays a protective role in the brain.
- TMEFF1 protein interacts with the HSV-1 receptor NECTIN-1, blocking the virus's ability to enter brain cells, but genetic deficiencies in TMEFF1 allow for easier viral entry and replication within neurons.
- The research suggests that enhancing TMEFF1 levels or using type I interferon can restore resistance to HSV-1, indicating a potential therapeutic pathway for preventing HSV-1 encephalitis.
Article Synopsis
- Aging is a significant risk factor for Alzheimer's disease, and researchers conducted a whole-genome CRISPR screen to find out how neuronal age is regulated.
- They discovered that the neddylation pathway affects both cellular aging and neurodegeneration related to Alzheimer's in human stem cells.
- Blocking neddylation led to more signs of aging and neuron loss, suggesting that targeting this pathway could be a new strategy to slow down Alzheimer's progression.