Antioxidants (Nutrients That Can Slow Alzheimer's)People need oxygen to live, but oxygen also has a downside. In the body, some oxygen molecules become so highly chemically reactive that they disrupt other body processes. These troublemaker molecules are called free radicals, and many scientists believe that the damage they inflict (oxidative damage) is at the root of both cancer and heart disease. (Smoking and a high-fat diet greatly increase the number of free radicals in the blood.) Free radicals may also contribute to the development of Alzheimer's disease. Beta-amyloid appears to react with the cells that line blood vessels in the brain to produce excessive quantities of free radicals, which damage brain tissue even more. Brain tissue is highly susceptible to free radical damage because, unlike many other tissues, it does not contain significant amounts of protective antioxidant compounds.(1) Fortunately, certain nutrients -- antioxidants -- might prevent the oxidative damage free radicals cause. Antioxidant nutrients include: Vitamin A, Vitamin C, Vitamin E (alpha-tocopherol, the most widely used one), the mineral selenium, the carotenoids (among them beta-carotene). These nutrients are abundant in plant foods, and curry might also have specific risk-reduction potential. A growing number of studies have investigated the effects of antioxidants on Alzheimer's disease. Results to date have been intriguing: Czech researchers gave the antioxidant drug selegiline to 173 people with mild to moderate Alzheimer's disease. After six months, their memory improved significantly. In another study, selegiline enhanced the benefits of tacrine (Cognex), one of the CEI drugs currently approved for Alzheimer's treatment.(2) Since the presence of metals has been postulated as contributing to AD,
and to oxidative "stress", the use of chelating agents has been
suggested as the focus of some research, but there doesn't seem to be
any rigorous research on that yet. Aluminum exposure has been studied
for 40 years because dialysis patients who build up aluminum in the bloodstream
sometimes develop a form of dementia. Studies have produced mixed results
on aluminum levels in the brains of AD patients. Efforts to correlate
aluminum levels with plaque density in AD patients have been inconclusive.
THere is no clear elevation of AD risk in people with occupational exposure
to aluminum. Nor is there an increased prevalence of AD in cultures that
drink lots of tea, yet tea leaves accumulate unusually large amounts of
aluminum that may leach into the drink. Vitamin E is being investigated in a large study of Mild Cognitive Impairments conducted by Ronald C. Petersen (Mayo Clinic) and Leon Thal (UC SanDiego), as one agent that might delay or stop memory deterioration before Alzheimer's has even been diagnosed.
Oxidative damage is the earliest event in Alzheimer disease.
Recently, this study demonstrated a significant increase of an oxidized
nucleoside derived from RNA, 8-hydroxyguanosine (8OHG), and an oxidized
amino acid, nitrotyrosine in vulnerable neurons of patients with Alzheimer
disease (AD). To determine whether oxidative damage is an early- or end-stage
event in the process of neurodegeneration in AD, they investigated the
relationship between neuronal 8OHG and nitrotyrosine and histological
and clinical variables, i.e. amyloid-beta (A beta) plaques and neurofibrillary
tangles (NFT), as well as duration of dementia and apolipoprotein E (ApoE)
genotype. The findings show that oxidative damage is quantitatively greatest
early in the disease and reduces with disease progression. They found
that increases in A beta deposition are associated with decreased oxidative
damage. These relationships are more significant in ApoE epsilon4
carriers. Moreover, neurons with NFT show a 40%-56% decrease in relative
8OHG levels compared with neurons free of NFT. Their observations indicate
that increased oxidative damage is an early event in AD that decreases
with disease progression and lesion formation. These findings suggest
that AD is associated with compensatory changes that reduce damage from
reactive oxygen. |