Possible Modification of Alzheimer Disease by Statins in Midlife: Interactions with Genetic and Non-Genetic Risk Factors
| Autor: | Mitsuru eShinohara, Naoyuki eSato, Hitomi eKurinami, Munehisa eShimamura, Toshimitsu eHamasaki, Amarnath eChatterjee, Hiromi eRakugi, Ryuichi eMorishita |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Apolipoprotein E
Gerontology Aging Statin medicine.drug_class Cognitive Neuroscience Disease Review Article Bioinformatics law.invention lcsh:RC321-571 Rotterdam Study Randomized controlled trial prevention law Alzheimer Disease Diabetes mellitus Medicine abeta Prospective cohort study lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry isoprenoids business.industry statin medicine.disease lipids (amino acids peptides and proteins) Alzheimer's disease business Alzheimer’s disease Neuroscience |
| Zdroj: | Frontiers in Aging Neuroscience, Vol 6 (2014) Frontiers in Aging Neuroscience |
| ISSN: | 1663-4365 |
| DOI: | 10.3389/fnagi.2014.00071/full |
| Popis: | The benefits of statins, commonly prescribed for hypercholesterolemia, in treating Alzheimer’s disease (AD) have not yet been fully established. A recent randomized clinical trial did not show any therapeutic effects of two statins on cognitive function in AD. Interestingly, however, the results of the Rotterdam study, one of the largest prospective cohort studies, showed reduced risk of AD in statin users. Based on the current understanding of statin actions and AD pathogenesis, it is still worth exploring whether statins can prevent AD when administered decades before the onset of AD or from midlife. This review discusses the possible beneficial effects of statins, drawn from previous clinical observations, pathogenic mechanisms, which include β-amyloid (Aβ) and tau metabolism, genetic and non-genetic risk factors (apolipoprotein E, cholesterol, sex, hypertension, and diabetes), and other clinical features (vascular dysfunction and oxidative and inflammatory stress) of AD. These findings suggest that administration of statins in midlife might prevent AD in late life by modifying genetic and non-genetic risk factors for AD. It should be clarified whether statins inhibit Aβ accumulation, tau pathological features, and brain atrophy in humans. To answer this question, a randomized controlled study using amyloid positron emission tomography (PET), tau-PET, and magnetic resonance imaging would be useful. This clinical evaluation could help us to overcome this devastating disease. |
| Databáze: | OpenAIRE |
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