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In JoVE (1)
Other Publications (3)
Articles by Laurent C. Delli-Bovi in JoVE
Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue
Jie Lu1, Laurent C. Delli-Bovi2, Jonathan Hecht3, Rebecca Folkerth4, Volney L. Sheen1
1Department of Neurology, Beth Israel Deaconess Medical Center, 2Department of Obstetrics and Gynecology, Brigham and Women's Hospital, 3Department of Pathology, Beth Israel Deaconess Medical Center, 4Department of Pathology, Division of Neuropathology, Brigham and Women's Hospital
A simple and reliable method on isolation and culture of neural stem cells from discarded human fetal cortical tissue is described. Cultures derived from known human neurological disorders can be used for characterization of pathological cellular and molecular processes, as well as provide a platform to assess pharmacological efficacy.
Other articles by Laurent C. Delli-Bovi on PubMed
Fetal Cell-free Plasma DNA Concentrations in Maternal Blood Are Stable 24 Hours After Collection: Analysis of First- and Third-trimester Samples
Clinical Chemistry. Jan, 2003 | Pubmed ID: 12507985
Contraception. Nov, 2007 | Pubmed ID: 17963861
This study evaluates the effectiveness of a community education campaign in the Boston community of Jamaica Plain conducted by the Massachusetts Emergency Contraception (EC) Network aimed at improving public knowledge of EC.
S100B and APP Promote a Gliocentric Shift and Impaired Neurogenesis in Down Syndrome Neural Progenitors
PloS One. 2011 | Pubmed ID: 21779383
Down syndrome (DS) is a developmental disorder associated with mental retardation (MR) and early onset Alzheimer's disease (AD). These CNS phenotypes are attributed to ongoing neuronal degeneration due to constitutive overexpression of chromosome 21 (HSA21) genes. We have previously shown that HSA21 associated S100B contributes to oxidative stress and apoptosis in DS human neural progenitors (HNPs). Here we show that DS HNPs isolated from fetal frontal cortex demonstrate not only disturbances in redox states within the mitochondria and increased levels of progenitor cell death but also transition to more gliocentric progenitor phenotypes with a consequent reduction in neuronogenesis. HSA21 associated S100B and amyloid precursor protein (APP) levels are simultaneously increased within DS HNPs, their secretions are synergistically enhanced in a paracrine fashion, and overexpressions of these proteins disrupt mitochondrial membrane potentials and redox states. HNPs show greater susceptibility to these proteins as compared to neurons, leading to cell death. Ongoing inflammation through APP and S100B overexpression further promotes a gliocentric HNPs phenotype. Thus, the loss in neuronal numbers seen in DS is not merely due to increased HNPs cell death and neurodegeneration, but also a fundamental gliocentric shift in the progenitor pool that impairs neuronal production.