Dementia prevention is the attempt to avoid developing dementia. Although there is no cure for dementia, there are ways to reduce the risk of developing dementia, including lifestyle changes and medications. Efforts to prevent dementia include trying to reduce risk factors for vascular disease, including diabetes, high blood pressure, obesity, smoking, and physical inactivity. “Use it or lose it” can be applied to the brain when it comes to dementia. Being mentally active helps keep your brain in shape for years to come. Reading, playing cards, board games, and playing a musical instrument are all examples of activities that can delay the onset and slow the progression of both Alzheimer’s and vascular dementia. The risk of developing dementia decreases with the frequency of these activities, and slower cognitive decline is associated with increased mental activity early in life and later in life. In addition to leisure activities, mentally demanding tasks may help prevent dementia, especially during the 30s, 40s, and 50s. Mental activity can help prevent dementia by building up “brain reserve”: additional connections between nerve cells that are more resistant to the deterioration associated with dementia. Since vascular dementia is the second most common form of dementia, reducing the risk of cerebrovascular disease also reduces the risk of dementia. Thus, exercising, having good cholesterol in the blood, maintaining a healthy weight and ideal blood pressure reduce the risk of dementia. An active lifestyle can reduce the risk by half compared to a sedentary life. And physical activity does not only affect the blood vessels, it can stimulate new neurons in the brain, in addition to releasing a substance that protects them. A protein known as neurotrophic factor (NDF) is known to be important for the growth, plasticity and survival of nerve cells. Regular exercise can boost levels by 2-3 times. Some studies suggest that high blood pressure is a cause of Alzheimer’s disease and other dementias, because it can cause blood vessel damage through constriction. Obesity increases the risk of any type of dementia and Alzheimer’s disease in particular. The effect of alcohol on the risk of dementia is represented by a J-curve, with higher alcohol consumption increasing the risk of dementia. While low alcohol consumption may be protective. However, low alcohol consumption may not protect against vascular dementia and cognitive decline in general. Moderate alcohol consumption may reduce the risk of vascular disease and dementia because it can increase levels of HDL cholesterol in the blood, impair blood clotting factors such as fibrinogen, and may provide some protection against heart attacks and mini-strokes that can damage the brain. The effect of omega-3 fatty acids in preventing dementia is also uncertain. Vegetables and nuts may be beneficial because of their high unsaturated fat content. Non-fish meats, on the other hand, increase the risk of Alzheimer’s disease because of their high saturated fat content. However, fish consumption should be limited due to concerns about mercury poisoning, which can worsen symptoms of dementia. Niacin is also believed to be effective in preventing dementia, and research has shown that those with the highest levels of niacin in their blood are believed to be at lower risk of developing dementia or cognitive decline. Niacin is involved in DNA synthesis and repair, nerve cell signaling, improves blood circulation and reduces cholesterol levels, and it is recommended that patients take 100-300 mg of niacin daily to benefit from its positive effects on the brain. There is evidence that there is a relationship between cognitive decline and homocysteine status, as well as B vitamins status, particularly vitamins B12, B6 and folic acid B9. In particular, a deficiency of vitamin B12 and/or folic acid can cause an increase in plasma homocysteine levels, which in turn leads to toxicity of the blood vessels and nervous system. Vitamin D deficiency has also been linked to cognitive impairment and dementia. However, the effect of vitamin D on cognitive impairment remains questionable. Sleeping more than nine hours a day may be associated with an increased risk of dementia. Poor sleep may also increase the risk of dementia by increasing the deposition of amyloid beta protein. Being neurotic increases the risk of Alzheimer's disease, a type of dementia. Neuroticism is associated with increased brain atrophy and cognitive impairment later in life, while conscientiousness has a protective effect against brain atrophy. High blood pressure is a risk factor for vascular dementia. Thus, lowering blood pressure with blood pressure-lowering medications may have a positive effect in preventing dementia, as may physical activity. However, one study failed to prove a link between high blood pressure and dementia. This study, published in July 2008 in The Lancet Neurology, found that blood pressure-lowering medications did not reduce the incidence of dementia to a statistically significant degree. Analysts of this and other studies suggested that further research could prove this. Diabetes is a risk factor for vascular dementia, and can be inhibited by antihyperglycemic agents. In addition, rosiglitazone improves memory and thinking abilities in people with early-stage Alzheimer's disease. The mechanism of this effect may be that the drug reduces insulin resistance and, therefore, the need for less insulin to metabolize it. Insulin in the bloodstream is the trigger for the production of amyloid beta, so lower levels of insulin in the bloodstream will lead to lower levels of these proteins. This leads to less amyloid plaque formation, which is closely associated with Alzheimer's disease and is seen in it. Estrogen may help prevent dementia, but not in the presence of dementia, when cognitive function is already impaired. This hormone increases blood flow to the brain and is an anti-inflammatory agent, which enhances the activity of synapses in the brain. This hormone may also help increase brain activation in areas affected by dementia, most commonly the hippocampus. There is limited evidence on the effects of estrogen that does not allow for a clear recommendation for estrogen supplementation, but it suggests that the timing of estrogen supplementation may be important, with early postmenopausal use preferred over later in life. NSAIDs have the potential to overcome risk factors for Alzheimer’s and Parkinson’s disease. The length of time needed to prevent dementia varies, but based on most studies, it is usually two to ten years. One study showed that these treatments must be used in a way that is appropriate to the patient’s clinical condition, and that so-called “baby aspirin” doses are ineffective in preventing and treating dementia. Alzheimer’s disease causes inflammation of neurons, which is caused by deposits of amyloid beta peptides in neurofibrillary tangles. These deposits irritate the body by causing the release of cytokines and acute phase proteins, for example, causing inflammation. As these substances accumulate over the years, they contribute to the effects of Alzheimer’s disease. NSAIDs prevent the formation of such inflammatory substances, preventing the effects from worsening. There is no vaccine for dementia yet. The explanation is that a vaccine could activate the body’s own immune system to fight the amyloid beta plaques in Alzheimer’s disease. One hurdle to overcome is an overreaction of the immune system, which causes inflammation of the brain.