Acrylamide (ACR) is a well-known neurotoxin in mammalian species that causes neuropathy characterized by ataxia and skeletal muscle weakness. Therefore, ACR-mediated axon damage in the central and peripheral nervous systems is considered to be central-peripheral axonopathy. However, the molecular mechanisms underlying ACR's toxicity to neural progenitor cells are unknown. This study investigated the adverse effects of ACR on mouse multipotent neural progenitor cells and adult hippocampal neurogenesis. ACR significantly reduced the proliferation of neural progenitor cells, and high ACR concentrations induced apoptotic and necrotic cell death. We found that elevated intracellular levels of reactive oxygen species were involved in ACR-mediated cytotoxicity. Interestingly, the administration of ACR to young mice resulted in a significant decrease in the number of newly generated cells in the dentate gyrus of the hippocampus, suggesting an impairment of adult neurogenesis. These results suggest that ACR's deleterious effects on the central nervous system are due to the death of neural progenitor cells and impaired adult neurogenesis.
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http://dx.doi.org/10.1016/j.toxlet.2009.12.015 | DOI Listing |
Cell Rep
January 2025
Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Erling Skjalgssons Gate 1, 7491 Trondheim, Norway; Kavli Institute for Systems Neuroscience and Centre for Algorithms in the Cortex, Norwegian University of Science and Technology, Olav Kyrres Gate 9, 7030 Trondheim, Norway. Electronic address:
The brain uses a specialized system to transport cerebrospinal fluid (CSF), consisting of interconnected ventricles lined by motile ciliated ependymal cells. These cells act jointly with CSF secretion and cardiac pressure gradients to regulate CSF dynamics. To date, the link between cilia-mediated CSF flow and brain function is poorly understood.
View Article and Find Full Text PDFStem Cell Reports
December 2024
Laboratorio di Biologia, Scuola Normale Superiore, 56126 Pisa, Italy; Istituto di Biofisica, Consiglio Nazionale delle Ricerche, 56124 Pisa, Italy. Electronic address:
The mechanisms that determine distinct embryonic pallial identities remain elusive. The central role of Wnt signaling in directing dorsal telencephalic progenitors to the isocortex or hippocampus has been elucidated. Here, we show that timely inhibition of MAPK/ERK and BMP signaling in neuralized mouse embryonic stem cells (ESCs) specifies a cell identity characteristic of the allocortex.
View Article and Find Full Text PDFCells
January 2025
Department of Chemistry, Biology and Biotechnologies, University of Perugia, Via dell'Elce di Sotto 8, 06123 Perugia, Italy.
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 PDFInt J Med Sci
January 2025
Department of Emergency Medicine, Chi Mei Medical Center, Tainan, Taiwan.
Effective therapies for cognitive impairments induced by brain irradiation are currently lacking. This study investigated the therapeutic potential of hyperbaric oxygen therapy (HBOT) for radiation-induced brain injury in a randomized controlled experimental model using adult male Wistar rats. Adult male Wistar rats were divided into four experimental groups: 0 Gy whole brain radiotherapy (WBRT) with normal baric air (NBA) treatment, 0 Gy WBRT with HBOT, 10 Gy WBRT with NBA, and 10 Gy WBRT with HBOT.
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