The Effects of Astaxanthin on Amyloid Beta Challenged Hippocampal Cell Growth and Mitochondrial Function During Hypoglycemia

Abstract

In the next 30 years, the amount of individuals diagnosed with Alzheimer's disease is expected to reach 30 million while the rate of diabetes mellitus is also projected to rise as well. In diabetes, hypoglycemia is a common consequence due to therapy. Previous research has shown a potential link between Alzheimer's disease and diabetes. This study sought to determine if Astaxanthin, ATX, could prevent mitochondrial dysfunction from the compounded effects of amyloid β (Aβ) plaque and hypoglycemia. Growth patterns, ATP production, and ROS generation were examined in 2 μM, 5 μM, 25 μM (hypoglycemic groups) and 2 mM or 5 mM glucose, and then treated with or without ATX or Aβ. When hypoglycemic groups were treated with ATX, their growth patterns were either comparable to or increased. ATX and Aβ monomers treated cells demonstrated increased growth patterns over hypoglycemic cells treated with Aβ monomers. Aβ alone treated groups overall had significantly less growth than controls (p < 0.05). Hypoglycemic groups produced overall low levels of ATP when ATP production was analyzed. Cells cultured with Aβ demonstrated low levels of average fluorescence generated by ROS production using the MitoSox assay while ATX groups actually produced higher to normal levels of ROS. Cells grown in the presence of Aβ and ATX generally produced more ROS than just Aβ groups. Thus, hypoglycemia does appear to compound the effects of Aβ monomers on hippocampal cells. ATX treatment demonstrated promise with increased cellular growth, which promotes usage of ATP by the cell and ROS production. This growth is also observed in the presence of Aβ and with other treatments may be useful in the treatment of these two disease states.