The Effect of Cold-Inducible Rna-Binding Protein (Cirp) on Phosphorylated Camkii Downregulation
Hannah Joseph
July 01, 2023
ISBN: 979-8-89480-841-3
Alzheimer’s Disease (AD) is an irreversible neurodegenerative disease which affects more than six million Americans. Although the etiology of AD is unclear, studies suggest alcohol consumption as a risk factor for dementia requiring neurologists’ aid. The prevalence of binge drinking worldwide is 16%. Research demonstrates binge drinking can release CIRP, a stress protein, from immune cells such as the microglia, to promote inflammation and inhibit neurological function. One essential function is synaptic plasticity. Synaptic plasticity, an important process of brain network development, relies on the activation of n-methyl-d-aspartate (NMDA) receptors. Activation of NMDA receptors results in calcium influx, most abundantly Calcium kinase II (CaMKII). Thus, this study measured phosphorylated CaMKII as an indicator of synaptic plasticity in HT-22 neuronal cell lines to determine CIRP’s effects on phosphorylated CaMKII downregulation. HT-22 cell lines were differentiated and separated into control, CIRP, CIRP + NMDA 10’, and CIRP + NMDA 30’ treatment groups. A NMDA control consisted of a control, NMDA 10’, NMDA 20’, and NMDA 30’ groups. These time intervals determined the ideal time of CIRP activation. Each CIRP treatment group was initially treated with CIRP and after four hours, designated groups were treated with NMDA in time intervals. After, tissue lysates were used for phosphorylated CaMKII protein quantification and western blot. The results demonstrate that CIRP did not significantly decrease phosphorylated CaMKII (p = 0.9781). This suggests CIRP did not effectively downregulate synaptic plasticity which would likeThe Effect of Cold-Inducible Rna-Binding Protein (Cirp) on Phosphorylated Camkii Downregulation Hannah Joseph ly induce AD. Future studies can use cells that exhibit neuronal properties to clearly identify CIRP’s effects.
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