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Congenital cytomegalovirus (cCMV) infection is associated with long-term central nervous system sequelae, including sensorineural hearing loss and neurodevelopmental delay, but mechanisms of neuropathogenesis in the developing fetal brain are incompletely understood. Animal models biologically representative of congenital infection have been used to characterize the effects of cCMV on neurogenesis, brain development, and cochlear development. Murine models utilizing host transcriptional analyses have been helpful in understanding the inflammatory response to cCMV infection and have demonstrated a correlation between elevation of proinflammatory mediators and altered brain and cochlear morphology during development. In this article, we review mechanisms of neuropathogenesis in cCMV animal models, with particular focus on the role of CMV-induced neuroinflammation in the impairment of fetal brain development.
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http://dx.doi.org/10.1093/jpids/piaf021 | DOI Listing |
BMC Psychiatry
September 2025
Zentrum Isartal Am Kloster Schäftlarn, Schäftlarn, Germany.
Background: Patients with mental health conditions represent a significant concern in emergency departments, consistently ranking as the third or fourth most prevalent diagnoses during consultations. Globally, over the past two decades, there was a marked increase in such incidences, largely driven by a rise in nonurgent visits related to somatic complaints. However, the implications of these nonurgent visits for mental health patients remain unclear, and warrant further investigation.
View Article and Find Full Text PDFBiochem Genet
September 2025
Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University Cerrahpasa, Kocamustafapasa, 34098, Istanbul, Turkey.
Glioblastoma is the most aggressive and malignant tumor of the central nervous system. Current treatment options, including surgical excision, radiotherapy, and chemotherapy, have Limited efficacy, with a median survival rate of approximately 15 months. To develop novel therapeutics, it is crucial to understand the underlying molecular mechanisms driving glioblastoma.
View Article and Find Full Text PDFNature
September 2025
Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA.
Neural activity is increasingly recognized as a crucial regulator of cancer growth. In the brain, neuronal activity robustly influences glioma growth through paracrine mechanisms and by electrochemical integration of malignant cells into neural circuitry via neuron-to-glioma synapses. Outside of the central nervous system, innervation of tumours such as prostate, head and neck, breast, pancreatic, and gastrointestinal cancers by peripheral nerves similarly regulates cancer progression.
View Article and Find Full Text PDFSignal Transduct Target Ther
September 2025
Spine & Spinal Cord Institute, Department of Neurosurgery, College of Medicine, Yonsei University, Seoul, Republic of Korea.
Neuroregeneration and remyelination rarely occur in the adult mammalian brain and spinal cord following central nervous system (CNS) injury. The glial scar has been proposed as a major contributor to this failure in the regenerative process. However, its underlying molecular and cellular mechanisms remain unclear.
View Article and Find Full Text PDFJ Neurosci
September 2025
Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, Nova Scotia, Canada, B3H4R2
At the glutamatergic synapses between rod photoreceptors and ON-type bipolar cells, neurotransmitter is detected by the postsynaptic metabotropic glutamate receptor mGluR6. This receptor forms trans-synaptic interactions with ELFN1, a presynaptic cell adhesion molecule expressed in rods, and ELFN1 is important for mGluR6 localization at bipolar cell dendritic tips. Here, we show that in mice of either sex lacking mGluR6, the presynaptic localization of ELFN1 is disrupted.
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