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Glaucomatous retinal ganglion cells: death and protection.
Int J Ophthalmol
January 2025
Department of Ophthalmology, the Second Affiliated Hospital of Xi'an Medical University, Xi'an 710038, Shaanxi Province, China.
Glaucoma is a group of diseases characterized by progressive optic nerve degeneration, with the characteristic pathological change being death of retinal ganglion cells (RGCs), which ultimately causes visual field loss and irreversible blindness. Elevated intraocular pressure (IOP) remains the most important risk factor for glaucoma, but the exact mechanism responsible for the death of RGCs is currently unknown. Neurotrophic factor deficiency, impaired mitochondrial structure and function, disrupted axonal transport, disturbed Ca homeostasis, and activation of apoptotic and autophagic pathways play important roles in RGC death in glaucoma.
View Article and Find Full Text PDFTDP-43 transports ferritin heavy chain mRNA to regulate oxidative stress in neuronal axons.
Neurochem Int
January 2025
Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan; Department of Neurotherapeutics, Osaka University Graduate School of Medicine, Osaka, Japan; Mount Fuji Research Institute, Yamanashi Prefectural Government, Yamanashi, Japan. Electronic address:
Amyotrophic lateral sclerosis (ALS) is characterized by the mislocalization and abnormal deposition of TAR DNA-binding protein 43 (TDP-43). This protein plays important roles in RNA metabolism and transport in motor neurons and glial cells. In addition, abnormal iron accumulation and oxidative stress are observed in the brain and spinal cord of patients with ALS exhibiting TDP-43 pathology and in animal models of ALS.
View Article and Find Full Text PDFAction potential-independent spontaneous microdomain Ca transients-mediated continuous neurotransmission regulates hyperalgesia.
Proc Natl Acad Sci U S A
January 2025
Department of Neurology, the Second Affiliated Hospital, Neuroscience Research Center, Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710000, China.
Neurotransmitters and neuromodulators can be released via either action potential (AP)-evoked transient or AP-independent continuous neurotransmission. The elevated AP-evoked neurotransmission in the primary sensory neurons plays crucial roles in hyperalgesia. However, whether and how the AP-independent continuous neurotransmission contributes to hyperalgesia remains largely unknown.
View Article and Find Full Text PDFRespiratory failure as main presentation sign of MAPT-related disorder.
J Neurol
January 2025
Centre de Génétique Humaine, Centre Hospitalier Universitaire de Besançon, Besançon, France.
Introduction: The MAPT gene encodes Tau, a protein mainly expressed by neurons. Tau protein plays an important role in cerebral microtubule polymerization and stabilization, in axonal transport and synaptic plasticity. Heterozygous pathogenic variation in MAPT are involved in a spectrum of autosomal dominant neurodegenerative diseases known as taupathies, including Alzheimer's disease, Pick's disease, fronto-temporal dementia, cortico-basal degeneration and progressive supranuclear palsy.
View Article and Find Full Text PDFImpaired Presynaptic Function Contributes Significantly to the Pathology of Glycine Receptor Autoantibodies.
Neurol Neuroimmunol Neuroinflamm
March 2025
Institute for Clinical Neurobiology, University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Background And Objectives: Autoantibodies (aAbs) against glycine receptors (GlyRs) are mainly associated with the rare neurologic diseases stiff person syndrome (SPS) and progressive encephalomyelitis with rigidity and myoclonus (PERM). GlyR aAbs are also found in other neurologic diseases such as epilepsy. The aAbs bind to different GlyR α-subunits and, more rarely, also to the GlyR β-subunit.
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