We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Alzheimer’s disease (AD) is a priority health problem devoid of curative treatment. The medication currently available includes acetylcholinesterase inhibitors (AChEIs)(donepezil, rivastigmine, galantamine, huperzine) and memantine. Only one new drug has been approved by the FDA in the last 17 years, so a shift in the paradigm of finding new treatments seems imperative. This involves a better understanding of AD pathogenesis, identifying predictive biomarkers, and customizing treatments. The implementation of pharmacogenomic procedures is an efficient option to optimize the scarce resources available and to accelerate the discovery of new treatments. The pharmacogenomic machinery is composed of pathogenic, mechanistic, metabolic, transporter and pleiotropic genes, under strict regulatory control of epigenetic mechanisms. Since dementia patients suffer from other concomitant diseases and receive up to 10 or more different medications, pharmacogenetics predicts therapeutic response, reduce drug interactions, and limit the adverse effects of anti-dementia drugs.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.