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Alzheimer's Disease - PreventionReduce CholesterolThe toxicity of beta amyloid (Aβ) is mainly mediated by lipid rafts which are membrane microdomains enriched in sphingolipids and cholesterol (see The Tau Protein). Higher level of cholesterol may increase the formation of lipid rafts, thereby facilitating Aβ toxicity. In a study on 9,844 participants, it has been found that the total cholesterol is associated with an increased risk of Alzheimer's Disease (AD) (reference). Increase Intellectual ActivitiesFor many years, it has been known that AD is associated with lower intellectual activities or less education (reference 1, reference 2). This result is very surprising, since AD typically starts from entorhinal cortex and hippocampus - the main brain regions involved in learning and memory. One would expect learning activities could somehow exacerbate AD. This puzzle is now solved by the finding that synaptic activity reduces intraneuronal Aβ through two mechanisms: (1) induce Aβ release into the extracellular space, and (2) activate the enzyme neprilysin to degrade intraneuronal Aβ (reference). As explained in The Tau Protein, intraneuronal Aβ is more toxic than extracellular Aβ because it can activate the enzyme GSK3β to phosphorylate Tau proteins at the axon initial segment, producing free phosphorylated Tau proteins which are the origin of AD. Dietary SupplementsDHA (docosahexaenoic acid): It is a type of healthy omega-3 fatty acid found in fish. DHA is associated with a reduced incidence of Alzheimer's disease, but it does not slow the progression from mild to moderate AD (reference). Therefore, DHA may be taken as a preventive supplement, not for treatment of AD. The beneficial effects of DHA could be related to its ability in suppressing Tau phosphorylation (reference). Melatonin: It is a hormone naturally produced by the pineal gland in the brain. This hormone has beneficial effects on a wide range of health problems, including Alzheimer's disease (reference). Melatonin is known to be a potent antioxidant, which can prevent oxidative damages resulting from calcium dysregulation.
Author: Frank Lee
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