Designing a Model to Explore Tau's Unfolded Protein Response
Poster Mar 07, 2018
Lauren Gould, Roy Blackburn, Laura J. Blair
It is known that the accumulation of the protein tau leads to neuronal loss that cause the mental deficits associated with AD. While tau’s relationship with increased neurotoxicity in the brain is known, the method as to how tau triggers the activation of the unfolded protein response (UPR) is unclear and has not been highly explored.
The purpose of this research is to design a cell model in which ER stress caused by tau accumulation can be generated, and then investigated for changes in different ER stress-associated proteins. The data provided by this experiment will allow for a working in vitro model of tau UPR and its effects on ER stress that will allow enhanced understanding of how tau causes neuronal death in AD.
Psychiatric Risk Gene Cacna1c and Early Life Stress: Potential Gene-Environment interactions?Poster
Early life stress (ELS) is highly associated with development of psychopathology
and mood disorders in adulthood. Genetic studies have identified variation in the gene calcium voltage-gated channel subunit alpha1C (CACNA1C) to increase risk for several psychiatric disorders. This poster assessed the expression of Cacna1c following prepubertal stress.
Regulatory T-Cells (Tregs) Within Bone Marrow-Derived Stem Cells (BMSCs) Actively Confer Immunomodulatory and Neuroprotective Effects Against StrokePoster
We found a distinct subpopulation of Tregs within BMSCs. Tregs and BMSCs in co-culture conferred neuroprotection that varied in a dose-dependent manner. Tregs minimized stem cell production of IL-6, a pro-inflammatory cytokine, and inhibited BMSC secretion of FGF-beta, a cytokine related to BMSC proliferation and differentiation. The ratio of Tregs found natively in BMSCs is optimally adapted to provide the maximum neuroprotective benefit of stem cell treatment after ischemic stroke.READ MORE
Comparing The Anti-Alzheimer's Activity of Different Types of CoffeePoster
This study found that coffee solutions treated at 5% are toxic to neurons. However, the toxicity reduced significantly at 2.5%. While the toxicity was significantly less allowing for more cells to survive at 2.5%, the levels of toxic amyloid beta 1-42 significantly reduced. This reduction in amyloid beta is associated with improvement in cognitive performance, as the presence of these toxic peptides is one of the characteristics of AD pathophysiology.READ MORE
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International Conference on Nanomedicine and Nanotechnology
Aug 20 - Aug 21, 2018