The study followed nearly 7,000 people age 55 and older for an average of seven years. Over that time, 706 of the participants developed dementia. People who were current smokers at the time of the study were 50 percent more likely to develop dementia than people who had never smoked or past smokers.
Smoking could affect the risk of dementia through several mechanisms, according to study author Monique Breteler, MD, PhD, of Erasmus Medical Center in Rotterdam, the Netherlands, and member of the American Academy of Neurology.
Smoking increases the risk of cerebrovascular disease, which is also tied to dementia, Breteler said. Another mechanism could be through oxidative stress, which can damage cells in the blood vessels and lead to hardening of the arteries. Smokers experience greater oxidative stress than nonsmokers, and increased oxidative stress is also seen in Alzheimer's disease.
Oxidative stress occurs when the body has too many free radicals, which are waste products produced by chemical reactions in the body.
Antioxidants in the diet can eliminate free radicals, and studies have shown that smokers have fewer antioxidants in their diets than nonsmokers, Breteler said.
The researchers also looked into how smoking affects the risk of developing Alzheimer's disease for people who have the gene that increases the risk of Alzheimer's, called apolipoprotein E4, or APOE 4. They found that smoking did not increase the risk of Alzheimer's for those with the APOE 4 gene. But for those without the APOE 4 gene, smoking increased the risk of Alzheimer's. Current smokers without the Alzheimer's gene were nearly 70 percent more likely to develop Alzheimer's than nonsmokers or past smokers without the Alzheimer's gene.
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After three days, the researchers compared the mice with normal OPN and the OPN-lacking mice. The normal OPN mice experienced weight loss, spleen and thymus atrophy, and a reduced number of white blood cells. In addition, increased levels of corticosterone, a steroid that contributes to the death of white blood cells, were found only in the normal OPN mice studied.
By contrast, the mice lacking the OPN gene showed statistically insignificant changes in weight and the levels of corticosterone, and were more similar to the control group.
White blood cell death in the spleen and thymus was evident only in the mice with normal OPN, Shi said. Since white blood cells were dying rather than increasing, that indicates partly why immune system organs atrophy during prolonged physical stress.
The team concluded that under chronic physical stress, OPN must be present for the increase in corticosterone, which leads to atrophy and white blood cell death.
Shi hopes that this finding will lead to preventative treatments in the future.
Already we're researching an antibody that can remove OPN from blood serum. Perhaps one day, we can turn this research into a therapy to counteract white blood cell death in immune system organs and keep humans healthier during times of prolonged physical stress, Shi said.
Shi and colleagues want to better understand the mechanisms through which stress affects the immune system, so they can prevent illness in space and help those who suffer from illness following physiological stress here on Earth.
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