TITLE:
Hypoglycemia, Hyperglycemia and Astaxanthin: An in Vitro Alzheimer’s Disease Model
AUTHORS:
Julie Griffith, Shauna Northup, Emma Cieslik, Marie Kelly-Worden
KEYWORDS:
ATP Luciferase Assay, ROS Production, Amyloid Beta, Astaxanthin, Diabetes Mellitus
JOURNAL NAME:
Advances in Alzheimer's Disease,
Vol.8 No.3,
September
30,
2019
ABSTRACT: Alzheimer’s Disease is projected to increase to 30 million people in the next 30 years and the rate of diabetes mellitus is projected to rise also. Hyperglycemia is commonly observed in patients with diabetes mellitus, and hypoglycemia is a common consequence due to insulin 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 or hyperglycemia. Growth patterns, ATP production, and ROS generation were examined in 2 μM, 5 μM, 25 μM (hypoglycemic groups), 2 mM, 5 mM (normal groups), and 25 mM glucose (hyperglycemic group), and then treated with or without ATX or Aβ. When hypoglycemia groups and the hyperglycemia group were treated with ATX, their growth patterns were either comparable to control or increased. ATX and Aβ treated cells demonstrated increased growth patterns over cells treated with Aβ alone. Aβ alone treated groups overall had significantly less growth than controls (p β demonstrated low levels of average fluorescence generated by ROS production as determined by 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 and hyperglycemia do appear to compound the effects of Aβ on hippocampal cells. ATX treatment demonstrated promise with increased cellular growth, which promoted usage of ATP by the cell and ROS production. This growth was present even in the presence of Aβ, suggesting that ATX is able to overcome the negative effects of Aβ.