There are many different type of antioxidant, each of which has a slightly different role; this makes talking about 'antioxidants' as a general term difficult, and especially difficult to measure. Though lab-based (in vitro) experiments on different types of antioxidants seem promising, there is only limited support for the claims that antioxidants may protect against Alzheimer's disease from studies involving people. However, increasing fresh fruit and vegetables in the diet has numerous benefits aside from increasing antioxidant intake and is highly recommended, especially as part of a Mediterranean diet.
Several studies suggest that 'oxidative stress' may play a role in the changes in the brain that cause Alzheimer's disease. Oxidative stress can lead to 'attack' on brain cells by chemicals called free radicals. It is these free radicals that cause oxidative damage. One study has shown that brains of people with Alzheimer's disease show lesions that are typically associated with free radical exposure.
Free radicals are produced by cells as a by-product of energy production, and therefore are a result of normal functioning. They have both harmful and beneficial effects in cells. Free radicals alter the structure and function of substances in the body. For example, in high concentrations they can damage proteins and DNA. They can damage cell membranes (the protective covering of cells), cause tissue damage and inflammation, and generally disrupt chemical processes within the body. To prevent this disruption and damage, our bodies naturally make, and acquire from food, molecules that react with free-radicals. These are generally called 'antioxidants'.
Different types of antioxidant
Huge numbers of different substances can act as antioxidants. Some of the most well known include vitamin C, vitamin E, beta-carotene and other related carotenoids, flavonoids, phenols, and many more. Putting all these chemicals into one large group is actually quite misleading. Each antioxidant has a different chemical composition, behaves slightly differently, and has a slightly different role. This makes it difficult to examine 'antioxidants' as a general and single aspect in dementia risk.
In the brain, free radicals seem to contribute to ageing and age-associated neurodegenerative disorders. The brain is particularly susceptible to oxidative damage as it uses lots of oxygen to produce energy, has high levels of unsaturated fatty acids (which are particularly susceptible to damage), and relatively low levels of antioxidants. There is substantial evidence that oxidative damage to the brain is an early event in Alzheimer's disease. Brains of people with Alzheimer's disease appear to have higher levels of natural antioxidants responsible for 'clearing up' excess free radicals, suggesting that the body is trying to combat this damage. Signs of oxidative stress are found not only in the brain, but also in the cerebral spinal fluid and the urine of people with Alzheimer's disease.
Many different types of antioxidant have been investigated in relation to Alzheimer's disease, but most experiments have been conducted in vitro (in the lab). For example, in vitro studies show antioxidants reduce the toxicity of amyloid-beta, but long-term studies in people have shown conflicting results.
There are lots of antioxidant supplements on the market claiming to have positive health benefits. However, a number of clinical trials looking into supplements have had to be stopped early due to participants experiencing adverse effects, such as higher rates of cancer development in those taking the antioxidant supplements. Other trials have shown that there does not appear to be a long term, detrimental effect of taking antioxidants.
Although the findings from studies are contradictory, the lack of certain benefits suggests that taking supplements may not be an advantage. It is important to note that these were trials on supplements - increasing your levels of antioxidants by increasing fresh fruit and vegetable consumption is associated with many long term benefits.