A 1998 study provides another intriguing clue to the origins of AD. This study, conducted by scientists from Oxford University and Norway's University of Bergen showed that blood levels of homocysteine (an amino acid) were significantly higher and blood levels of folate were lower in patients with diagnosed AD than in controls (Clarke et al., 1998). The study's authors suggest that high levels of homocysteine might be a risk factor for AD.
Recent findings from the Nun Study also suggest a link between folate and brain dysfunction. In this research, investigators determined blood levels of folate and other nutrients from selected nuns living in a convent in Mankato, Minnesota (Snowdon et al., in press). They then compared these folate levels with the degree of AD pathology present in the brains of any nuns who died. All of the participating nuns ate from the same kitchen and lived similar lives. Examinations of the brains of 30 nuns who have died since the beginning of the study showed that the neocortex–one of the primary regions of the brain affected in AD–of those who had low blood folate levels showed significant shrinkage, and that the correlation was particularly evident among 15 nuns who had many AD plaques and tangles. None of the other nutrients examined showed the same correlations. Folate, also called folic acid, plays an important role in the development of the central nervous system (CNS) and may play a role in maintaining its integrity throughout life. One of folate's functions, along with vitamins B6 and B12, is to convert homocysteine to the more useful amino acid methionine. High levels of homocysteine have been linked in epidemiologic studies to risk of heart disease, and, in the study by Clarke and colleagues, to risk of AD.
Source: National Institutes of Health; National Institute on Aging
1999 PROGRESS REPORT ON ALZHEIMER'S DISEASE