Neural stem cells (NSCs) are characterized by a capacity for self-renewal, differentiation into multiple neural lineages, all of which are considered to be promising components for neural regeneration. However, for cell-replacement therapies, it is essential to monitor the process of in vitro NSC differentiation and identify differentiated cell phenotypes. We report a real-time and label-free method that uses a capacitance sensor array to monitor the differentiation of human fetal brain-derived NSCs (hNSCs) and to identify the fates of differentiated cells. When hNSCs were placed under proliferation or differentiation conditions in five media, proliferating and differentiating hNSCs exhibited different frequency and time dependences of capacitance, indicating that the proliferation and differentiation status of hNSCs may be discriminated in real-time using our capacitance sensor. In addition, comparison between real-time capacitance and time-lapse optical images revealed that neuronal and astroglial differentiation of hNSCs may be identified in real-time without cell labeling.
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http://dx.doi.org/10.1038/srep06319 | DOI Listing |
Alzheimers Dement
December 2024
Brown University, Providence, RI, USA.
Background: Chitinase-3-like protein 1 (CHI3L1, or YKL-40) is an important regulator of immunity and, in the brain, is primarily secreted by activated astrocytes and heralds a neurotoxic inflammatory state. While it has been well known as a high-profile biomarker for Alzheimer's disease (AD) and inflammatory brain conditions (e.g.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, USA.
Background: Sleep disturbances are associated with the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD) and primary tauopathies. We have previously shown that APOE4, the strongest genetic risk factor for AD, directly influences the severity of key pathological hallmarks of neurodegeneration including tau deposition, microglial reactivity and brain atrophy. Sleep loss influences tau accumulation and microglial reactivity in both mice and humans, suggesting that sleep loss may contribute to neurodegeneration not only by influencing protein aggregation, but also through an immune mechanism.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
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View Article and Find Full Text PDFMol Neurobiol
December 2024
Department of Emergency Medicine, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
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View Article and Find Full Text PDFNeuron
December 2024
Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. Electronic address:
Transient exposure to ketamine can trigger lasting changes in behavior and mood. We found that brief ketamine exposure causes long-term suppression of futility-induced passivity in larval zebrafish, reversing the "giving-up" response that normally occurs when swimming fails to cause forward movement. Whole-brain imaging revealed that ketamine hyperactivates the norepinephrine-astroglia circuit responsible for passivity.
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