Astaxanthin Attenuates Neurotoxicity in a Mouse Model of Parkinson’s disease
Poster Feb 13, 2017
Grimmig. B., Daly. L., Hudson. C., Nash. K., Bickford. PC
Astaxanthin (AXT) is a natural carotenoid with diverse biological activities. Although it is best known as a potent antioxidant, recent work suggests additional mechanisms of action that have the potential to oppose the ongoing pathophysiology of Parkinson’s Disease (PD). For example, AXT has a putative role in modulating microglial activity and preserving mitochondrial function, thus supporting the role of this compound as a neuroprotective agent. Both oxidative stress and inflammation are involved in the progression of many neurodegenerative diseases, therefore, we examined the potential for AXT to reduced neurotoxicity in a toxic model of PD in mice. Here, we show that administration of algae derived AXT mitigated MPTP induced dopamine cell death. After a four week dietary supplementation, AXT treated mice were protected against the loss of tyrosine hydroxylase (TH) positive cells in the substantia nigra (SN) after MPTP exposure (10 mg/kg administered hourly for a total of 40mg/kg) compared to the control diet. This effect of preserved TH immunoreactivity was also observed in the striatum. Furthermore, AXT administration was able to interrupt the neuroinflammatory process known to contribute to neurodegeneration in this model. We demonstrate that AXT neuroprotection was associated with attenuated microglial activation indicated by reduced immunohistochemical detection of IBA-1 in the SN and striatum of AXT treated mice. Taken together, these studies suggest that AXT has neuroprotective property in the CNS against MPTP neurodegeneration.
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.
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