Our group previously reported that soluble TNF (sTNF) modulates cytokine and chemokine cascades that regulate peripheral immune cell traffic to the brain in young 5xFAD female mice, and in separate studies that a diet high in fat and sugar (HFHS) dysregulates signaling pathways that trigger sTNF-dependent immune and metabolic responses that can result in metabolic syndrome, which is a risk factor for AD. The cytokine tumor necrosis factor (TNF) is elevated in AD patients, regulates brain and gut barrier permeability, and is produced by central and peripheral immune cells. Signaling between peripheral immune cells and those within the microvasculature and meninges of the central nervous system (CNS), at the blood-brain barrier, and in the gut likely plays an important role in AD. ![]() The immune system is a major contributor mediating these interactions. Introduction: Increasing evidence indicates that neurodegenerative diseases, including Alzheimer’s disease (AD), are a product of gene-by-environment interplay. 5Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, United States.4Department of Neuroscience and Center for Translational Research in Neurodegenerative Disease, The University of Florida College of Medicine, Gainesville, FL, United States.3Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY, United States. ![]()
0 Comments
Leave a Reply. |