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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 787805, 9 pages
Research Article

Calcium Channel Blockers, Progression to Dementia, and Effects on Amyloid Beta Peptide Production

1Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
2Sanders-Brown Center on Aging and Alzheimer’s Disease Center, University of Kentucky, Lexington, KY 40536, USA
3Department of Epidemiology, University of Kentucky, Lexington, KY 40506, USA
4Departments of Statistics and Biostatistics, University of Kentucky, Lexington, KY 20536, USA
5National Minority Quality Forum, Washington, DC 20005, USA

Received 22 February 2015; Revised 5 June 2015; Accepted 8 June 2015

Academic Editor: Ada Popolo

Copyright © 2015 Mark A. Lovell et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Previous epidemiologic studies suggest that antihypertensive drugs may be protective against cognitive decline. To determine if subjects enrolled in the University of Kentucky longitudinal aging study who used antihypertensive drugs showed diminished progression to dementia, we used a 3-parameter logistic regression model to compare the rate of progression to dementia for subjects who used any of the five common categories of antihypertensive drugs to those with similar demographic characteristics but who did not use antihypertensives. Regression modeling showed that subjects who used calcium channel blockers (CCBs) but not the other classes of antihypertensives showed a significant decrease in the rate of progression to dementia. Significantly, use of CCBs ameliorated the negative effects of the presence of APOE-4 alleles on cognitive decline. To determine if CCBs could minimize amyloid beta peptide (Aβ1–42) production, H4 neuroglioma cultures transfected to overexpress APP were treated with various CCBs and Aβ1–42 levels and levels of proteins involved in Aβ production were quantified. Results show that treatment with nifedipine led to a significant decrease in levels of Aβ1–42, with no significant decrease in cell viability. Collectively, these data suggest that use of CCBs significantly diminishes the rate of progression to dementia and may minimize formation of Aβ1–42.