Alzheimer's disease (AD) is characterized by dementia and memory loss that is associated with extracellular senile plaques of amyloid precursor protein derived amyloid-beta (Aβ) protein and intracellular neurofibrillary tangles consisting of the Tau protein (Scheltens et al., 2016). A primary in vitro model of AD is therefore treatment of cells with Aβ peptide that causes cytotoxicity to both primary cultures of neurons as well as neuronal cell lines. Treatment of primary cortical neuron cultures derived from Wistar rat embryos with tauroursodeoxycholic acid (TUDCA) prior to exposure to Aβ peptide significantly decreased nuclear fragmentation and cytochrome c release that was dependent upon activation of the PI3K pathway (Solá et al., 2003). The bile acid UDCA was found to regulate IκBα and NF-κB regulated genes in the mechanism of protection against Aβ toxicity in the BV-2 microglial cell line (Joo et al., 2004).