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Increased reactive oxygen species (ROS) generation and the ensuing oxidative stress contribute to Alzheimer's disease pathology. We reported previously that amyloid- β  peptide oligomers (A β Os) produce aberrant Ca 2+  signals at sublethal concentrations and decrease the expression of type-2 ryanodine receptors (RyR2), which are crucial for hippocampal synaptic plasticity and memory. Here, we investigated whether the antioxidant agent astaxanthin (ATX) protects neurons from A β Os-induced excessive mitochondrial ROS generation, NFATc4 activation, and RyR2 mRNA downregulation. To determine mitochondrial H 2 O 2  production or NFATc4 nuclear translocation, neurons were transfected with plasmids coding for HyperMito or NFATc4-eGFP, respectively. Primary hippocampal cultures were incubated with 0.1  μ M ATX for 1.5 h prior to A β Os addition (500 nM). We found that incubation with ATX (≤10  μ M) for ≤24 h was nontoxic to neurons, evaluated by the live/dead assay. Preincubation with 0.1  μ M ATX also prevented the neuronal mitochondrial H 2 O 2  generation induced within minutes of A β Os addition. Longer exposures to A β Os (6 h) promoted NFATc4-eGFP nuclear translocation and decreased RyR2 mRNA levels, evaluated by detection of the eGFP-tagged fluorescent plasmid and qPCR, respectively. Preincubation with 0.1  μ M ATX prevented both effects. These results indicate that ATX protects neurons from the noxious effects of A β Os on mitochondrial ROS production, NFATc4 activation, and RyR2 gene expression downregulation.

Astaxanthin Protects Primary Hippocampal Neurons against Noxious Effects of Aβ-Oligomers