Does Estrogen Act as a Neuroprotective Agent on In Vitro‐Induced β‐Amyloid Plaques in N38 Hypothalamic Neuronal Cells?

Abstract

A key characteristic of Alzheimer's disease (AD) is the deposition of beta‐amyloid fibrils in extracellular plaques, as well as the intracellular accumulation of tau in neurofibrillary tangles in the brain. This study is designed to induce plaques on N38 hypothalamic neuronal cells under in vitro conditions using synthetic beta‐amyloid and subsequently to treat with estrogen as a neuroprotective reagent. The cell viability, toxicity and proliferation were determined using different bioassays like cell count, Congo red, MTT and lactate dehydrogenase assay. Results indicate a significant loss in cell death, amyloidosis, mitochondrial dysfunction and increased cytotoxicity in cells treated with beta‐amyloid and neuroprotection when exposed to estrogen. Further, in order to understand the mechanism by which neuronal death by plaque formation and neuroprotection by estrogen western blotting was performed to determine the changes associated with biomarker Tau protein. Taking together the biochemical and molecular data, the neuroprotective effect of estrogen on beta amyloid plaque formation will be analyzed.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.