Abstract
The translation of promising preclinical treatments into effective drugs for Alzheimer's disease (AD) has been challenging.One of the most potent risk factors for sporadic AD is carrier status of the epsilon 4 allele of the apolipoprotein E gene (E4). E4 carriersshow a differential response to several therapies which are being investigated as AD treatments, including acetylcholinesterase inhibitorsand therapeutics with vascular and metabolic targets. The differential treatment responses of E4 carriers may partially explain why sometreatments show a null effect in clinical trials. Understanding the reasons behind these responses is not only important for clinical practice,but may also help us elucidate mechanisms for this neurodegenerative disease.
Keywords:Alzheimer's disease, treatments, APOE genotype.
Current Pharmaceutical Design
Title:The APOE Genotype: Modification of Therapeutic Responses in Alzheimer's Disease
Volume: 21Issue: 1
Author(s):Angela J. Hanson, Suzanne Craft and William A. Banks
Affiliation:
Keywords:Alzheimer's disease, treatments, APOE genotype.
Abstract: The translation of promising preclinical treatments into effective drugs for Alzheimer's disease (AD) has been challenging.One of the most potent risk factors for sporadic AD is carrier status of the epsilon 4 allele of the apolipoprotein E gene (E4). E4 carriersshow a differential response to several therapies which are being investigated as AD treatments, including acetylcholinesterase inhibitorsand therapeutics with vascular and metabolic targets. The differential treatment responses of E4 carriers may partially explain why sometreatments show a null effect in clinical trials. Understanding the reasons behind these responses is not only important for clinical practice,but may also help us elucidate mechanisms for this neurodegenerative disease.
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Cite this article as:
Hanson Angela J., Craft Suzanne and Banks A. William, The APOE Genotype: Modification of Therapeutic Responses in Alzheimer's Disease, Current Pharmaceutical Design 2015; 21 (1) .https://dx.doi.org/10.2174/1381612820666141020164222
| DOI https://dx.doi.org/10.2174/1381612820666141020164222 | Print ISSN 1381-6128 |
| Publisher Name Bentham Science Publisher | Online ISSN 1873-4286 |
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