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Cecchi, C., Nichino, D., Zampagni, M., Bernacchioni, C., Evangelisti, E., Pensalfini, A., Liguri, G., Gliozzi, A., Stefani, M. and Relini, A. (2009) A Protective Role for Lipid Raft Cholesterol against Amyloid-Induced Membrane Damage in Human Neuroblastoma Cells. Biochimica et Biophysica Acta, 1788, 2204-2216.
has been cited by the following article:
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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.