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Virus-mediated delivery of single-chain antibody targeting TDP-43 protects against neuropathology, cognitive impairment and motor deficit caused by chronic cerebral hypoperfusion.
Exp Neurol
January 2025
CERVO Brain Research Centre, Québec, Québec G1J 2G3, Canada; Department of Psychiatry and Neuroscience, Université Laval, Québec City G1V 0A6, Canada. Electronic address:
Chronic cerebral hypoperfusion induced by permanent unilateral common carotid artery occlusion in mice was recently found to induce an age-dependent formation of insoluble cytoplasmic TDP-43 aggregates reminiscent of pathological changes found in human vascular dementia. In this model, the gradual deregulation of TDP-43 homeostasis in cortical neurons was associated with marked cognitive and motor deficits. To target the TDP-43-mediated toxicity in this model, we generated an adeno-associated virus vector encoding a single-chain antibody against TDP-43, called scFv-E6, designed for pan-neuronal transduction following intravenous administration.
View Article and Find Full Text PDFFirst Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis.
Brain Sci
December 2024
College of Life Science and Engineering, Foshan University, 18 Jiangwan Street, Foshan 528231, China.
(), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that infection induces severe neuropathology in the brain manifested by increased nitric oxide production, oxidative stress, glial activation/BBB damage, increased pro-inflammatory cytokine glia maturation factor-beta and induced apoptosis. The aim of this experimental study was to investigate the serum amyloid P (SAP) components, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), caspase 1 (Casp 1), tumor necrosis factor-alpha (TNF-α) and complement 3 (C3) gene expressions on the 10th, 20th and 30th days after infection with in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) in mouse brains by real-time quantitative polymerase chain reaction.
View Article and Find Full Text PDFLithium restores nuclear REST and Mitigates oxidative stress in down syndrome iPSC-Derived neurons.
Neuroscience
January 2025
Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, UPM, Serdang, Selangor, Malaysia; Malaysian Research Institute on Ageing (MyAgeing(TM)), Universiti Putra Malaysia, 43400, UPM, Serdang, Selangor, Malaysia. Electronic address:
Article Synopsis
- Down syndrome (DS) is linked to trisomy 21, leading to intellectual disabilities and increased oxidative stress, impacting neuronal health.
- REST is a key protein involved in regulating genes related to DS neuropathology, and this study explores lithium’s effects on restoring REST levels in DS neurons.
- Results indicated that lithium treatment restored nuclear REST levels and significantly reduced reactive oxygen species (ROS) in DS neurons, suggesting potential therapeutic benefits of lithium for improving neuronal function in Down syndrome.
Immune cell infiltration and modulation of the blood-brain barrier in a guinea pig model of tuberculosis: Observations without evidence of bacterial dissemination to the brain.
PLoS One
December 2024
Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, is a chronic inflammatory disease. Although typically associated with inflammation of the lungs and other peripheral tissues, increasing evidence has uncovered neurological consequences attributable to Mtb infection. These include deficits in memory and cognition, increased risk for neurodegenerative disease, and progressive neuropathology.
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