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The Neuroprotective Effects of Estrogen in an Alzheimer’s Disease Hypothalamic Cell Line
Author(s) -
Hindieh Jennifer Grace,
Persaud Nikita,
Cooperstein Deborah,
Chakraborty Tandra R.,
Chakraborty Sanjoy
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.04155
Subject(s) - neuroprotection , estrogen , viability assay , cell culture , intracellular , amyloid beta , mtt assay , western blot , chemistry , pharmacology , amyloid (mycology) , microbiology and biotechnology , cell , biology , medicine , endocrinology , biochemistry , pathology , disease , genetics , gene
Alzheimer’s Disease (AD), is a neurodegenerative disease affecting memory and cognition, eventually leading to dementia. Two of the most notable hallmarks of AD are the aggregation and depositing of beta‐amyloid fibrils as extracellular plaques as well as the intracellular accumulation of Tau as neurofibrillary tangles in the brain. Research suggests a possible neuroprotective role of the female sex hormone estrogen in neurodegenerative diseases, including AD. Using established AD cell line SH‐SY5Y as a control and N38 hypothalamic cells as an experimental cell line, AD will be modeled in vitro by incubating with synthetic, oligomerized beta‐amyloid, and subsequently, treating the culture with estrogen to observe its efficacy as a neuroprotective reagent. A western blot assay will be used to confirm the presence of total tau, before and after treatment. We hypothesize that cells treated with Aβ42 will express larger amounts of total Tau in contrast to cells treated with both estrogen and amyloid. Preliminary results confirm the presence of Tau in SH‐SY5Y and N38 cell line. Tau‐46 was used as the primary antibody, GAM‐HRP as a secondary antibody, with GADPH used as a control. Supplemental bioassays, MTT and LDH, were performed to determine cell viability, cytotoxicity, and proliferation. Preliminary results in MTT with N38 cells showed that Aβ42 reduced mitochondrial activity within 24hrs. These results also indicated estrogens’ neuroprotective capabilities within hypothalamic cells by counteracting the negative effect of Aβ42. Through analysis of both quantitative and qualitative data, there will be further clarification of the possible neuroprotective nature of estrogen with regards to beta amyloid plaque toxicity. Support or Funding Information Adelphi University & New York City College of Technology