Neuroprotective effects of estrogen on Alzheimer induced SH‐SY5Y neuroblastoma cells and N38 hypothalamic neuronal cells

Abstract

Alzheimer's disease is a neurodegenerative disease characterized by neuronal cell damage and death, neurofibrillary tangle formation and cerebral plaques formed by beta amyloid peptides. Previous studies have shown that the hippocampus, a region of brain related to cognition and memory is mainly affected by Alzheimer's disease. This study is designed to induce Alzheimer's disease by treating SH‐SY5Y neuroblastoma cells and N38 hypothalamic neuronal cells with synthetic beta‐amyloid plaques under in vitro conditions. In the current study, we wanted to determine whether hypothalamus; a region involved in feeding, sleep, reproduction and energy balance is affected similarly as well. Hypothalamic cells were treated with beta‐amyloid1‐42 to induce neurofibrillary tangles and plaque formation. The cell viability, toxicity and proliferation were determined using different bioassays like cell count, MTT and lactate dehydrogenase assay. Preliminary results indicated a significant loss in mitochondrial function when exposed to beta‐amyloid. Cell damage and cellular toxicity were further analyzed by lactate dehydrogenase (LDH). Further, western blotting was done to determine the changes associated with biomarkers like P53 and Tau protein. Taking together the biochemical and molecular data the neuroprotective effect of estrogen on beta amyloid plaque formation will be analyzed.Support or Funding InformationAdelphi UniversityThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.