Publications by authors named "Amennai D Beyeen"
Article Synopsis
- Parent-of-origin effects involve various genetic and epigenetic mechanisms in inheritance, which have been linked to the development of multiple sclerosis (MS) and similar conditions.
- A study using rats with experimental autoimmune encephalomyelitis (EAE) revealed that 37-54% of disease-predisposing genetic loci are influenced by which parent they are inherited from, with a notable role played by the Y chromosome.
- The research highlights that certain genes, particularly on chromosome 6, exhibit imprinting patterns affecting disease severity, suggesting that understanding these epigenetic contributions could improve the identification of risk factors for MS and related diseases.
Genetic mapping on fully sequenced individuals is transforming understanding of the relationship between molecular variation and variation in complex traits. Here we report a combined sequence and genetic mapping analysis in outbred rats that maps 355 quantitative trait loci for 122 phenotypes. We identify 35 causal genes involved in 31 phenotypes, implicating new genes in models of anxiety, heart disease and multiple sclerosis.
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- - Multiple sclerosis (MS) is a genetic disease that causes inflammation in the central nervous system and can be studied using a model called experimental autoimmune encephalomyelitis (EAE), which has shown a link between specific genetic markers and the severity of this condition in lab rats.
- - Researchers created a special rat strain that integrates a specific genetic region associated with a reduced severity of EAE, finding that these rats experienced milder disease symptoms and less damage to their nerves compared to the typical susceptible strain.
- - The study revealed that the congenic rats had increased levels of certain chemokines (like CCL11) in their lymph nodes and spinal cords, contributing to a stronger immune response and a healthier blood-brain barrier
Multiple sclerosis (MS) is an inflammatory neurodegenerative disease of the CNS. Recent advances in whole-genome screening tools have enabled discovery of several MS risk genes, the majority of which have known immune-related functions. However, disease heterogeneity and low tissue accessibility hinder functional studies of established MS risk genes.
View Article and Find Full Text PDFGenetic regulation of autoimmune neuroinflammation is a well known phenomenon, but genetic influences on inflammation following traumatic nerve injuries have received little attention. In this study we examined the inflammatory response in a rat traumatic brain injury (TBI) model, with a particular focus on major histocompatibility class II (MHC II) presentation, in two inbred rat strains that have been extensively characterized in experimental autoimmune encephalomyelitis (EAE); DA and PVG. In addition, MHC and Vra4 congenic strains on these backgrounds were studied to give information on MHC and non-MHC gene contribution.
View Article and Find Full Text PDFBackground: To elucidate mechanisms involved in multiple sclerosis (MS), we studied genetic regulation of experimental autoimmune encephalomyelitis (EAE) in rats, assuming a conservation of pathogenic pathways. In this study, we focused on Eae23, originally identified to regulate EAE in a (LEW.1AV1xPVG.
View Article and Find Full Text PDFMultiple sclerosis, the most common cause of progressive neurological disability in young adults, is a chronic inflammatory disease. There is solid evidence for a genetic influence in multiple sclerosis, and deciphering the causative genes could reveal key pathways influencing the disease. A genome region on rat chromosome 9 regulates experimental autoimmune encephalomyelitis, a model for multiple sclerosis.
View Article and Find Full Text PDFDefinition of dysregulated immune components in multiple sclerosis may help in the identification of new therapeutic targets. Deviation of the interleukin 18 receptor 1 (IL18R1) is of particular interest since the receptor is critical for experimental neuroinflammation. The objective of this study was to determine whether expression of IL18R1 varies between multiple sclerosis patients and controls, and to test genetic association of IL18R1 with multiple sclerosis.
View Article and Find Full Text PDFWe here present the first genetic fine mapping of experimental autoimmune neuritis (EAN), the animal model of Guillain-Barré syndrome, in a rat advanced intercross line. We identified and refined a total of five quantitative trait loci on rat chromosomes 4, 10, and 12 (RNO4, RNO10, RNO12), showing linkage to splenic IFN-gamma secretion and disease severity. All quantitative trait loci were shared with other models of complex inflammatory diseases.
View Article and Find Full Text PDFThe laboratory rat (Rattus norvegicus) is a key tool for the study of medicine and pharmacology for human health. A large database of phenotypes for integrated fields such as cardiovascular, neuroscience, and exercise physiology exists in the literature. However, the molecular characterization of the genetic loci that give rise to variation in these traits has proven to be difficult.
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