[This corrects the article DOI: 10.18632/oncotarget.18053.].
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6281412 | PMC |
| http://dx.doi.org/10.18632/oncotarget.26387 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Modifying reaction time tasks parameters in the automated IntelliCage identifies heightened impulsivity and impaired attention in the 3xTg-AD model of Alzheimer's disease.
Front Aging Neurosci
December 2024
Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, United States.
Background: The 3xTg-AD transgenic mouse model of Alzheimer's disease (AD) is an important tool to investigate the relationship between development of pathological amyloid-β (Aβ) and tau, neuroinflammation, and cognitive impairments. Traditional behavioral tasks assessing aspects of learning and memory, such as mazes requiring spatial navigation, unfortunately suffer from several shortcomings, including the stress of human handling and not probing species-typical behavior. The automated IntelliCage system was developed to circumvent such issues by testing mice in a social environment while measuring multiple aspects of cognition.
View Article and Find Full Text PDFThe Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.
Int J Biol Sci
January 2025
Department of Neonatology and Pediatric Intensive Care, Children's Hospital University of Bonn, Bonn, Germany.
Article Synopsis
- Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of death and disability in newborns, and caffeine has shown promise in mitigating its effects.
- In a neonatal rat model, caffeine administration post-injury reduced brain damage and inflammation compared to controls, highlighting its potential benefits.
- The study found that caffeine influences the AMPK/mTOR pathway, suggesting that targeting this pathway could enhance neuroprotection and improve outcomes for HIE, especially in regions lacking sufficient resources for treatment.
Engineered tRNAs efficiently suppress CDKL5 premature termination codons.
Sci Rep
December 2024
Department of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan), 20054, Italy.
Article Synopsis
- The CDKL5 deficiency disorder (CDD) is a severe neurodevelopmental condition with symptoms including early epilepsy, intellectual disabilities, and motor/visual dysfunction, caused by mutations in the CDKL5 gene.
- Currently, there is no cure for CDD; treatments focus on managing seizures, though some genetic therapies show promise in addressing the disorder's root causes.
- Recent studies using Anticodon-edited tRNAs (ACE-tRNAs) have shown potential in restoring full-length CDKL5 protein synthesis, opening up possibilities for effective new treatments for patients with nonsense mutations.
Role of in Filamentous Growth and Pathogenicity of .
J Fungi (Basel)
November 2024
Key Laboratory of Microbiological Metrology, Measurement & Bio-Product Quality Security, State Administration for Market Regulation, College of Life Sciences, China Jiliang University, Hangzhou 310018, China.
is a dimorphic fungus that specifically infects , causing stem swelling and the formation of an edible fleshy stem known as jiaobai. The pathogenicity of is closely associated with the development of jiaobai and phenotypic differentiation. Msb2 acts as a key upstream sensor in the MAPK (mitogen-activated protein kinase) signaling pathway, playing critical roles in fungal hyphal growth, osmotic regulation, maintenance of cell wall integrity, temperature adaptation, and pathogenicity.
View Article and Find Full Text PDFComprehensive analysis of peripheral blood free amino acids in MASLD: the impact of glycine-serine-threonine metabolism.
Amino Acids
December 2024
Department of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Little is known about how blood free amino acids (FAAs) change in metabolic dysfunction-associated steatotic liver disease (MASLD). This study aims to identify the imbalance of FAAs in MASLD and explore its correction as a potential therapeutic target. We analyzed plasma FAAs data from 23,036 individuals with steatosis information from a biobank in Japan, and 310 patients with MASLD were enrolled.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!