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http://dx.doi.org/10.1007/BF00351773 | DOI Listing |
F1000Res
January 2025
Faculty of Teaching and Education Sciences, Islamic University of Malang, Malang, East Java, Indonesia.
Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.
View Article and Find Full Text PDFBiomed Opt Express
January 2025
Department of Biomedical Engineering, University of Illinois Chicago, Chicago, IL 60607, USA.
The choroid, a critical vascular layer beneath the retina, is essential for maintaining retinal function and monitoring chorioretinal disorders. Existing imaging methods, such as indocyanine green angiography (ICGA) and optical coherence tomography (OCT), face significant limitations, including contrast agent requirements, restricted field of view (FOV), and high costs, limiting accessibility. To address these challenges, we developed a nonmydriatic, contrast agent-free fundus camera utilizing transcranial near-infrared (NIR) illumination.
View Article and Find Full Text PDFHypertens Res
January 2025
Department of Pharmacology, Ehime University Graduate School of Medicine, Shizugawa, Japan.
Sci Transl Med
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Antiamyloid antibody treatments modestly slow disease progression in mild dementia due to AD. Emerging evidence shows that homeostatic dysregulation of the brain immune system, especially that orchestrated by microglia, plays an important role in disease onset and progression.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91052 Erlangen, Germany.
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation.
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