Scienceblogtwo

According to a group of researchers from UTHealth Houston, a recently created agonistic antibody reduced the amyloid pathology in mice with Alzheimer's disease, indicating its promise as a potential treatment for the condition. Researchers at McGovern Medical School at UTHealth Houston, under the direction of senior author Zhiqiang An, PhD, professor and holder of the Robert A. Welch Distinguished University Chair in Chemistry, discovered that a tetra-variable domain antibody directed against the triggering receptor expressed on myeloid 2 (TREM2), known as TREM2 TVD-lg, reduced amyloid burden, eased neuronal damage, and lessened cognitive decline in mice with Alzheimer's disease Today, Science Translational Medicine published the study. An, head of the Texas Therapeutics Institute at The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, stated that "antibody-based therapy is a promising pharmacological approach for the treatment of Alzh...

The LSU Health New Orleans Neuroscience Center, the Departments of Cell Biology and Anatomy, Neurology, and Ophthalmology have collaborated on research led by Drs. Yuhai Zhao and Walter J. Lukiw that describes for the first time a pathway that starts in the gut and ends with a powerful pro-inflammatory toxin in brain cells that contributes to the onset of Alzheimer's disease (AD). They also describe a straightforward approach to stop it. Results are accessible here in Frontiers in Neurology. The scientists discovered proof that a neurotoxic known as BF-LPS is produced in the human gastrointestinal (GI) tract by a molecule comprising an extremely potent microbially produced neurotoxin (lipopolysaccharide, or LPS), which is obtained from the Gram-negative bacteria Bacteroides fragilis. According to Dr. Lukiw, LPSs are likely the most potent pro-inflammatory, neurotoxic glycolipids generated by microbes. Numerous labs, including our own, have found various LPS subtypes in the neurons ...