Journal of Neuroscience paper shows that thromboxane receptor antagonists reduced plaque formation in mice.
Researchers found that the thromboxane receptor, which is activated by isoprostanes, may be a new therapeutic target for Alzheimer’s disease (AD). Previous studies have shown that two isoprostane isoforms are know to be elevated in AD and AD-like diseases but not in other neurodegenerative diseases.
Investigators found that injection of one of these isoprostanes increased the number of amyloid plaques in a mouse model of AD. They further showed that activation of the thromboxane receptor increased levels of amyloid precursor protein (APP) and its cleavage products including those that form plaques. The thromboxane receptor also increased the stability of APP mRNA and this likely provides more substrate for amyloid production, according to the researchers.
The scientists also showed that thromboxane receptor antagonists reversed the effects of isoprostane injection in mice and also reduced plaque formation in Tg2576 mice that were not treated with isoprostane.
The researchers involved in this study were from the University of Pennsylvania School of Medicine and Temple University. The study is published in the April 30 issue of the Journal of Neuroscience.
