Publications by authors named "G Alexandra"
Article Synopsis
- The study investigates how diabetes can lead to lung damage due to inflammation and explores the potential protective role of Vitamin D against this damage.
- Thirty rats were divided into groups to test different doses of Vitamin D and measure inflammation-related gene expressions in lung tissues.
- Results indicated that higher Vitamin D doses significantly reduced harmful inflammation markers in the lungs of diabetic rats, suggesting Vitamin D may help mitigate lung damage caused by diabetes.
Introduction: Various human viruses have been identified in wild monkeys and in captive primates. Cases of transmission of viruses from wild monkeys to humans and vice versa are known. The aim of this study was to identify markers of anthroponotic viral infections in vervet monkeys ( ) arrived from their natural habitat (Tanzania).
View Article and Find Full Text PDFBackground: We conducted an analysis to check whether the ABO blood group impacts the susceptibility or protection against different types of head and neck cancers.
Method: We analyzed the medical records of 61,899 cancer patients from "Prof. Dr.
Mislocalization of the predominantly nuclear RNA/DNA binding protein, TDP-43, occurs in motor neurons of ~95% of amyotrophic lateral sclerosis (ALS) patients, but the contribution of axonal TDP-43 to this neurodegenerative disease is unclear. Here, we show TDP-43 accumulation in intra-muscular nerves from ALS patients and in axons of human iPSC-derived motor neurons of ALS patient, as well as in motor neurons and neuromuscular junctions (NMJs) of a TDP-43 mislocalization mouse model. In axons, TDP-43 is hyper-phosphorylated and promotes G3BP1-positive ribonucleoprotein (RNP) condensate assembly, consequently inhibiting local protein synthesis in distal axons and NMJs.
View Article and Find Full Text PDFArticle Synopsis
- ALS is a deadly neurodegenerative disease marked by the degeneration of motor neurons, with mutations in CRMP4 linked to its progression.
- Research indicates that changes in CRMP4 levels contribute to the death of motor neurons, as its protein is found to be higher in cell bodies but lower in distal axons of affected neurons.
- The harmful mislocalization of CRMP4 due to its interaction with the dynein motor protein is a key factor in promoting motor neuron loss, suggesting that targeting this interaction could help reduce cell death in ALS models.