All pathophysiological mechanisms involved in the onset and progression of Alzheimer’s disease (AD) are related to oxidative stress1<\/sup>. Today, the amyloid beta (A\u03b2) cascade is the main hypothesis to explain the etiology of the disease. Deposits and accumulation of A\u03b2 leads to extracellular plaques, which have been postulated to be more protective than damaging in terms of oxidative stress. More than a decade ago we reasoned that damage due to A\u03b2 might be caused not by extracellular, but rather intracellular A\u03b2 peptide interacting with normal cell metabolism. A\u03b2 binds to heme and therefore partially blocks the passage of \u00e9lectrons through the respiratory chain and, as a consequence, the production of ROS is increased, thus we can propose a mechanism by which ROS are produced inside cells by interaction with A\u03b2 peptide. Radical production in turn causes mitochondria to aggregate and then they release cytochrome c which is a well-known activator of the endogenous pathway of apoptosis2<\/sup>. The increased ROS production results in oxidative stress which provides the basis for a putative treatment of AD with antioxidants.<\/p>\n Antioxidant enzymes are over-expressed in hippocampus and parietal lobule but not in cerebellum in AD3<\/sup>. This can be a mechanism to prevent partially the occurrence of ROS in AD. In fact, activating the expression of the antioxidant enzymes is always a good strategy to prevent oxidative stress and therefore partially prevent the occurrence and progression of AD.<\/p>\n Many clinical trials have been developed to clarify whether antioxidants are beneficial in AD treatment. However, the results obtained in no way confirm that antioxidants are an effective AD therapy. Even though major efforts have been made in determining whether antioxidant supplementation could be a means of preventing, or even treating, AD this idea is far from being established. In this line, vitamin E has been suggested as a powerful antioxidant and thus may cause beneficial effects and lower the progression of AD. A decisive paper published in 19974<\/sup> reported that vitamin E supplementation resulted in an improvement in the frailty of the patients but these authors did not observe a clear effect on cognition. We performed a study to correlate the administration of vitamin E to AD patients with the progression of the disease and with the blood oxidative stress status. We found that vitamin E does not cause a reduction of glutathione redox ratio in all patients. In those in whom it does not (non-respondent) vitamin E results in an even more pronounced loss of cognition than in patients treated with a placebo. For the patients who experimented a reduction in oxidative stress, cognition was maintained or slightly improved in the six months of the duration of the study5<\/sup>. We termed this the vitamin E paradox in Alzheimer\u2019s disease. The paradox is the fact that for some patients, vitamin E could even be detrimental whereas for others vitamin E treatment partially prevents the loss memory associated with the progression of the disease.<\/p>\n Moreover, the Rotterdam Study included 5,395 participants who were monitored for the incidence of dementia during ten years and had dietary assessment. The authors concluded that high dietary intake of vitamin C and E may lower the risk of AD6<\/sup>. But a more extensive analysis of the Rotterdam Study data (after multivariate adjustment) revealed that dietary intake levels of vitamin C were not associated with the risk of dementia and higher intake of foods rich in vitamin E may only modestly reduce AD7<\/sup>.<\/p>\n We can state that healthy habits like correct nutrition based on vegetables containing vitamins, particularly vitamins C and E, as well as modest changes in lifestyle towards a healthier one like increasing daily exercise which activate the expression of antioxidant enzymes are beneficial in preventing onset, and more importantly to delay the progression of Alzheimer\u2019s disease. Thus, as a final conclusion, we recommend nutritional and physiological changes that activate the expression of antioxidant defenses rather than taking antioxidant vitamins as means of preventing Alzheimer\u2019s disease.<\/p>\n","protected":false},"template":"","class_list":["post-71128","article_revue","type-article_revue","status-publish","hentry"],"acf":{"auteur":"","source":"","revue":[{"ID":70499,"post_author":"22","post_date":"2020-04-21 14:56:13","post_date_gmt":"2020-04-21 12:56:13","post_content":"","post_title":"68 - June 2012","post_excerpt":"","post_status":"publish","comment_status":"closed","ping_status":"closed","post_password":"","post_name":"68-june-2012","to_ping":"","pinged":"","post_modified":"2020-04-21 14:56:13","post_modified_gmt":"2020-04-21 12:56:13","post_content_filtered":"","post_parent":0,"guid":"https:\/\/aprifel-pp.mentalworks.biz\/?post_type=revue&p=70499","menu_order":254,"post_type":"revue","post_mime_type":"","comment_count":"0","filter":"raw"}],"position":"1","references":"Antioxidant treatment in Alzheimer\u2019s disease<\/h1>\n
Conclusions<\/h1>\n
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