The identification of strategies for the isolation of neural stem cells (NSCs) has important implications for the understanding of their biology and the development of therapeutic applications. It has been previously described that human neural stem and progenitor cells (NSPCs) can be isolated from the central nervous system (CNS) using antibodies to prominin (CD133) and fluorescence-activated cell sorting (FACS). Although this antigen displayed an identical membrane topology in several human and murine tissues there was uncertainty as to the relationship between human and mouse prominin because of the low level of amino acid identity. Here we show that prominin expression can be used to identify and isolate also murine NSPCs from the developing or adult brain. Prominin is co-expressed with known neural stem markers like SOX 1-2, Musashi and Nestin. Moreover, neurosphere-forming cells with multipotency and self-renewal capacity reside within the prominin-positive fraction. Transplantation experiments show that CD133-positive cells give rise to neurons and glial cells in vivo, and that many neurons display appropriate phenotypic characteristics of the recipient tissues. The demonstration that CD133 is a stem cell antigen for murine NSPCs as it is for human NSPCs is useful for the investigation of mammal neurogenesis and development of preclinical tests of NSPCs transplantation in mouse analogues of human diseases.
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http://dx.doi.org/10.1016/j.expneurol.2007.03.021 | DOI Listing |
Neurotherapeutics
January 2025
School of Pharmacy and Pharmaceutical Sciences, Cardiff University, King Edward VII Avenue, Cardiff, CF10 3NB, UK; Leibniz-Institut für Polymerforschung Dresden, Max Bergmann Center of Biomaterials Dresden, Hohe Straße 6, D-01069 Dresden, Germany. Electronic address:
Replacing cells lost during the progression of neurodegenerative disorders holds potential as a therapeutic strategy. Unfortunately, the majority of cells die post-transplantation, which creates logistical and biological challenges for cell therapy approaches. The cause of cell death is likely to be multifactorial in nature but has previously been correlated with hypoxia in the graft core.
View Article and Find Full Text PDFNeuropsychologia
January 2025
Department of Criminology & Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat Gan 5290002, Israel; Department of Neuroscience and Biomedical Engineering, Aalto University, Finland 00076. Electronic address:
While decreasing negative attitudes against outgroups are often reported by individuals themselves, biased behaviour prevails. This gap between words and actions may stem from unobtrusive mental processes that could be uncovered by using neuroimaging in addition to self-reports. In this study we investigated whether adding neuroimaging to a traditional intergroup bias measure could detect intersubject differences in intergroup bias processes in a societal context where opposing discrimination is normative.
View Article and Find Full Text PDFNeuron
January 2025
Department of Genetics, Stanford University, Stanford, CA, USA; Glenn Center for the Biology of Aging, Stanford University, Stanford, CA, USA; Wu Tsai Neurosciences Institute, Stanford University, Stanford, CA, USA. Electronic address:
Brain aging leads to a decline in cognitive function and a concomitant increase in the susceptibility to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. A key question is how changes within individual cells of the brain give rise to age-related dysfunction. Developments in single-cell "omics" technologies, such as single-cell transcriptomics, have facilitated high-dimensional profiling of individual cells.
View Article and Find Full Text PDFCurr Neurol Neurosci Rep
January 2025
Department of Neurosurgery, Gui de Chauliac Hospital, Montpellier University Medical Center, 80 Avenue Augustin Fliche, Montpellier, 34295, France.
Purpose Of Review: In low-grade glioma (LGG), besides the patient's neurological status and tumor characteristics on neuroimaging, current treatment guidelines mainly rely on the glioma's genetics at diagnosis to define therapeutic strategy, usually starting with surgical resection. However, this snapshot in time does not take into account the antecedent period of tumor progression and its interactions with the brain before presentation. This article reviews new concepts that pertain to reconstruct the history of previous interplay between the LGG's course and adaptive changes in the connectome within which the glioma is embedded over the years preceding the diagnosis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Massachusetts Medical School, Worcester, MA, USA.
Background: Neuron-derived extracellular vesicles (NDEVs) are a valuable resource for understanding brain conditions and discovering neurodegenerative diseases biomarkers, notably Alzheimer's disease (AD). Recent interest focuses on capturing neuron-specific EVs from patient-derived samples, characterizing their contents as a pathological reflection of the central nervous system (CNS). Our recent study identified ATPase Na/K Transporting Subunit Alpha 3 (ATP1A3) as a prevalent neuron-specific EV marker specifically expressed in brains.
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