BALTIMORE, MARYLAND. Age-related cognitive decline has been linked to raised levels of homocysteine in several population-based studies. Homocysteine is a sulfur-containing amino acid derived from methionine, which participates in protein metabolism and other essential processes. Homocysteine is also associated with cardiovascular and cerebrovascular disease, and cardiovascular and central nervous system health may be closely related. Therefore, researchers from Johns Hopkins University set out to verify the link in a large study, taking into account many related variables such as ethnicity and socioeconomic status.
The researchers randomly selected 1,140 participants aged 50 to 70 taking part in the ongoing Baltimore Memory Study. Blood samples were taken to determine homocysteine level, and blood pressure was measured. The participants were then interviewed and given 20 neurobehavioral tests to assess a broad range of cognitive abilities. A homocysteine level of greater than 15 umol (micromoles) per liter is considered elevated, and among the participants, levels ranged from 4.4 to 48.6 umol per liter. Results showed that high homocysteine levels were "consistently and strongly associated with poorer neurobehavioral test performance in crude analysis". This link remained after taking into account many related variables, and was found in each of the cognitive domains assessed.
The closest links were found between homocysteine level and simple motor and psychomotor speed, eye- hand coordination/manual dexterity, and verbal memory and learning. Further analysis showed that the difference in test scores from the 25th to the 75th percentile of homocysteine levels could be compared with an increase of 4.2 years of age. Participants in the highest fourth for homocysteine level were twice as likely to be in the lowest fourth for performance.
The results also suggest that the link between homocysteine level and cognitive performance may be
modified by the protein apolipoprotein E, with certain genotypes producing a greater effect. As the
magnitude of the associations was large, the researchers conclude that homocysteine may be a potentially
important modifiable cause of cognitive decline. Homocysteine can be reduced through increased intake of
folic acid and other B vitamins, especially vitamin B6 and vitamin B12.