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http://dx.doi.org/10.1055/a-2292-2013 | DOI Listing |
Heliyon
December 2024
Institute of Virology, Philipps-University Marburg, 35043, Marburg, Germany.
[This corrects the article DOI: 10.1016/j.heliyon.
View Article and Find Full Text PDFCommun Biol
January 2025
Division of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Changes in brain mitochondrial metabolism are coincident with functional decline; however, direct links between the two have not been established. Here, we show that mitochondrial targeting via the adiponectin receptor activator AdipoRon (AR) clears neurofibrillary tangles (NFTs) and rescues neuronal tauopathy-associated defects. AR reduced levels of phospho-tau and lowered NFT burden by a mechanism involving the energy-sensing kinase AMPK and the growth-sensing kinase GSK3b.
View Article and Find Full Text PDFZhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
December 2024
Department of Occupational and Radiological Diseases, Changzhou Center for Disease Prevention and Control, Changzhou 213022, China.
This paper reports two cases of occupational severe toxic encephalopathy caused by inhaling excessive nitrogen in an accident. The main reasons are failure to performing field-work standards of limited space operation and emergency rescue. Hypoxia asphyxia is the main pathogenic link of nitrogen toxicity, which can cause brain edema.
View Article and Find Full Text PDFEpilepsia
December 2024
Department of Neuroscience and Medical Genetics, Children's Hospital Meyer IRCCS, Florence, Italy.
Objective: Fenfluramine (FFA), stiripentol (STP), and cannabidiol (CBD) are approved add-on therapies for seizures in Dravet syndrome (DS). We report on the long-term safety and health care resource utilization (HCRU) of patients with DS treated with FFA under an expanded access program (EAP).
Methods: A cohort of 124 patients received FFA for a median of 2.
Cell Death Differ
December 2024
Georgetown University Medical Center, Lombardi Comprehensive Cancer Center, Washington, D.C., USA.
Germline inactivating mutations of the SLC25A1 gene contribute to various human disorders, including Velocardiofacial (VCFS), DiGeorge (DGS) syndromes and combined D/L-2-hydroxyglutaric aciduria (D/L-2HGA), a severe systemic disease characterized by the accumulation of 2-hydroxyglutaric acid (2HG). The mechanisms by which SLC25A1 loss leads to these syndromes remain largely unclear. Here, we describe a mouse model of SLC25A1 deficiency that mimics human VCFS/DGS and D/L-2HGA.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!