The molecular pathways that contribute to the onset of symptoms in tauopathy models, including Alzheimer’s disease (AD), are difficult to distinguish because multiple changes can happen simultaneously
We utilized a Caenorhabditis elegans (C. elegans) model of human tauopathy to investigate the role of DNA glycosylases (Ung-1 and Nth-1 knockout worms) in disease development and progression. We then
RNA sequencing of cortex from young (3mo) and old (10mo) P301S tau transgenic mice Overall design: 3 biological replicas per age and genotype (transgenic and non-transgenic)
Alzheimer’s disease (AD) is a heterogeneous disorder with multiple etiologies. Harnessing the immune system by blocking the programmed cell death receptor (PD)-1 pathway in an amyloid beta mouse model
