Thus, investigations of the effects of Aβ, cholesterol and ApoE isoforms on alterations of CECs' membrane biophysics, including imbalance in cell-cell adhesion, tight junctions integrity, CECs' endocytosis, and other important aspects of cell functions, would provide insights into the mechanisms of neuroinflammation in AD, their correlations with cardiovascular disorders, and may offer new therapeutic strategies for AD patients. This evidence concerns the gene APOE and Alzheimer disease.