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http://dx.doi.org/10.1111/j.1939-1676.2010.0518.x | DOI Listing |
J Vet Intern Med
December 2024
Unit of Diagnostic Imaging, Centre Hospitalier Vétérinaire ADVETIA, Vélizy-Villacoublay, France.
Background: Arterial spin labeling (ASL) is a noninvasive brain perfusion magnetic resonance imaging (MRI) technique that has not been assessed in dogs with meningoencephalitis of unknown origin (MUO).
Hypothesis/objectives: Assess brain perfusion changes characteristics before and after medical treatment, and investigate the role of ASL perfusion in the diagnosis and prognosis of MUO in dogs.
Animals: Thirty-one dogs with presumed MUO.
Pediatr Neurol
December 2024
Neurology Service, Department of Paediatrics, KK Women's and Children's Hospital, Singapore, Singapore. Electronic address:
Background: Bilateral hemorrhagic thalamic lesions in dengue encephalitis resemble lesions seen in acute necrotizing encephalopathy (ANE). We investigate whether dengue-associated ANE (DANE) should be considered an ANE variant or a mimic.
Methods: Systematic review of dengue encephalitis literature from PubMed and SCOPUS (inception to December 31, 2022).
Int J Mol Sci
October 2024
Department of Neurology, Juntendo University, Tokyo 1138431, Japan.
This study aimed to explore the intricate relationship between mitochondrial dysfunction, infection, and neuroinflammation, focusing specifically on the impact of pathogenic epitopes of the Epstein-Barr Virus (EBV) nuclear antigen 1 (EBNA1) in a mouse model of mitochondrial dysfunctions. The investigation included female middle-aged and C57BL/6J wild-type mice immunized with EBNA1 or with active experimental autoimmune encephalomyelitis (EAE) induction by the myelin oligodendrocyte glycoprotein (MOG) peptide. The mice developed more severe EAE than the wild-type mice.
View Article and Find Full Text PDFQual Life Res
December 2024
National Centre for Neuroimmunology and Emerging Diseases, Griffith University, 1 Parklands Drive, Southport Gold Coast, Brisbane, QLD, 4222, Australia.
Brain Behav Immun
November 2024
Institute of Physiology I, University of Münster, Münster, Germany. Electronic address:
Background: Multiple Sclerosis (MS) is an autoimmune neurodegenerative disease, whose primary hallmark is the occurrence of inflammatory lesions in white and grey matter structures. Increasing evidence in MS patients and respective murine models reported an impaired ionic homeostasis driven by inflammatory-demyelination, thereby profoundly affecting signal propagation. However, the impact of a focal inflammatory lesion on single-cell and network functionality has hitherto not been fully elucidated.
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