Kopf Carrier #72 • October 2011
Resveratrol therapy for Alzheimer’s disease
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Introduction In 1993, the first FDA-approved drug for treating the neural or chemical deficiencies that underlie Alzheimer’s disease (AD) was ushered into the clinical field of age-related dementias. Unfortunately, the drug, Tacrine (Cognex), has not been effective in reducing dementia, nor the disease progression (Fan et al., 2010). Given these and other limitations of current drug therapies, neuroscientists have been forced to search for new therapeutic strategies that might affect the underlying mechanisms of the disease. One such strategy is to treat the afflicted AD brain with resveratrol, a natural polyphenol found in grapes and red wine (Torres et al., 2008; Torres et al., 2011). In this brief review, we summarize the putative causes of AD, list the current therapeutic approaches to AD and discuss the rationale for using resveratrol in this and other neurodegenerative diseases. The disease: Clinical symptoms Alzheimer’s disease is a progressive neurodegenerative disorder with a prevalence of |
approximately 5% of the USA population over the age of 65 (Grabowski, 2011). Afflicted individuals suffer from blunted cognitive ability and as the disease progresses, severe memory loss, disorientation and aphasia become more symptomatic. In the later stages of AD, the patient becomes severely disabled, immobile and mute. Death occurs mostly from inanition, malnutrition and/or pneumonia (Grabowski, 2011). Conclusive diagnosis of the disease is made post-mortem, with certain aberrant histopathological findings noted throughout the brain parenchyma (Fauzi et al., 2008). However, due to advanced computer-based neuroimaging techniques (e.g., high-resolution structural MRI scans) and sophisticated behavioral testing (e.g., Mini-Mental State Examination), most cases of AD can now be correctly diagnosed in vivo by well-trained neurologists (Kumar et al., 2010). Pathology: Faulty brain circuits Considerable evidence suggests that AD is multifactorial, involving several different etiopathogenic mechanisms. When the AD brain is examined post-mortem using highly-specific histopathological stains and |