Elevated homocysteine associated with doubling of women's Alzheimer's disease risk
A thesis composed by Dr Dimitri Zylberstein at the Sahlgrenska Academy at the University of Gothenburg, Sweden links high levels of homocysteine in women with twice the risk of developing Alzheimer's disease compared to those with low levels.
Dr Zylberstein reports the results of a study involving participants in the Prospective Population Study of Women in Gothenburg, which enrolled nearly 1,500 subjects between the ages of 38 and 60 at the end of the 1960s. Blood samples obtained upon enrollment were analyzed for levels of serum homocysteine, an amino acid byproduct of metabolism which has been linked to an increased risk of cardiovascular disease and dementia when elevated. The women were followed for 35 years, making it the longest study to evaluate the relationship between homocysteine level and dementia.
"Alzheimer's disease was more than twice as common among the women with the highest levels of homocysteine than among those with the lowest, and the risk for any kind of dementia was 70 per cent higher," revealed Dr Zylberstein. "These days, we in our clinical practice use homocysteine analyses mainly for assessment of vitamin status. However, our results mean that we could use the very same analysis for assessment of individual's risk profile for dementia development. This opens the possibility for future preventive treatment at a very early stage."
It is not known whether increased homocysteine contributes to dementia or is elevated by a factor associated with the condition. Although elevated homocysteine can be the result of vitamin B12 and folate deficiencies, it can also occur when vitamin status is considered normal according to current standards.
Dr Zylberstein's thesis also examined a gene variant that is associated with a 65 percent lower risk of dementia when two copies are present, and with a 40 percent lower risk when one copy is present. "We have only been able to carry out a genetic analysis on just over 550 of the blood samples from the Prospective Population Study of Women, and want to undertake bigger studies before we can say for sure that the gene really does protect against dementia," stated professor Lauren Lissner, who supervised the thesis. "We hope to be able to perform the same analysis on more samples from the study."
Alzheimer’s disease is characterized by two key abnormalities: amyloid plaques and neurofibrillary tangles. Amyloid plaques are clumps of a protein known as beta-amyloid. These plaques are found in the tissue between nerve cells in the brain and in degenerating pieces of neurons.
Genetic factors clearly play a role. The disease runs in families, and several genes have been identified that raise the risk of Alzheimer’s disease (Kasper DL et al 2004). One such abnormality affects a lipid (fat) called apolipoprotein E (apoE). There are three types of apoE. People who have one particular type of apoE (apoE4) are more likely than other people to develop Alzheimer’s disease. Even this knowledge, however, is of limited use because the presence or absence of apoE in any form is not a strong enough indicator to justify using apoE4 as a widespread screening tool.
Compelling and growing evidence links inflammation and oxidative stress to Alzheimer’s disease. According to the inflammation theory (discussed in dozens of recent clinical trials), inflammatory cytokines gather at the neurons of people who have Alzheimer's.
Other possible causes include high levels of homocysteine in the brain and specific nutrient deficiencies. Although these ideas are still developing, they have opened up exciting new targets for therapy. In clinical studies, the most cutting-edge researchers are turning to therapies such as anti-inflammatory nutrients, antioxidants that reduce oxidative stress, and metal chelating agents (such as green tea) that reduce the levels of free iron in the brain.
Folic acid is needed for DNA synthesis and to make S-adenosylmethionine (SAMe). A study of 126 patients, including 30 who had Alzheimer’s disease, found that the levels of folate in cerebrospinal fluid were significantly lower in patients with late-onset Alzheimer’s disease (Serot JM et al 2001). Another longitudinal analysis of people between the ages of 70 and 79 years found that people who had high levels of homocysteine or low levels of folate had impaired cognitive function.
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