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Evans, R.M., Emsley, C.L., Gao, S., Sahota, A., Hall, K.S., Farlow, M.R. and Hendrie, H. (2000) Serum Cholesterol, APOE Genotype, and the Risk of Alzheimer’s Disease: A Population-Based Study of African Americans. Neurology, 54, 240-242.
https://doi.org/10.1212/WNL.54.1.240

has been cited by the following article:

• TITLE: Experimental Analysis of Interacting HT22 Plasma Membrane Cholesterol and β-Amyloid

  AUTHORS: George Livadiotis, Leila Assas, Maher A. Dayeh, Saber Elaydi, Chloe Phea, James L. Roberts, Yara Samman, Rachel Tchen

  KEYWORDS: Alzheimer Disease, β-Amyloid, Cholesterol

  JOURNAL NAME: Advances in Alzheimer's Disease, Vol.6 No.4, December 25, 2017

  ABSTRACT: The peptide β-Amyloid (β-A) is known to be one of the primary factors causing neurodegeneration in the Alzheimer disease. Hence, one would like to know the factors that would increase or decrease the toxicity of β-Amyloid in the brain. One of the factors that are debated in the literature is cholesterol, where it is not clear if modulating the levels of cholesterol would affect the degree of toxicity of β-Amyloid on neuron cells in the brain. In order to investigate this problem, data were collected and analyzed for three types of experiments: 1) Correspondence between cholesterol and methyl-β-cyclodextrin (MβCD) measurements; 2) measurements of the relative fluorescence unit (RFU) with respect to MβCD concentration (with/without β-A); and 3) RFU measurements with respect to β-A concentration (with/without MβCD). HT22 hippocampal neurons immortalized with the simian virus SV-40 large T-antigen plasmid vector were used to conduct the experiments. Mito-ID Membrane potential cytotoxicity was used as a measure of mitochondrial potential change. The statistical analysis of the presented experimental results indicates that cholesterol has no statistically significant effect on the degree of toxicity of β-Amyloid.