Examples of homocysteine

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Homocysteine potentiates beta-amyloid neurotoxicity : role of oxidative stress.
While white-matter hyperintensities had significant correlations with both homocysteine and depressive symptoms, the brain measures and total antioxidant capacity did not emerge as significant mediating variables.
Association between high homocysteine and ischaemic stroke due to largeand small-artery disease but not other aetiologic subtypes of ischaemic stroke.
A noteworthy finding of our study was the gender difference in the relationship of homocysteine with depression, which was significant for men but not for women.
Furthermore, attention should be paid to homocysteine levels in depressive illness and its prophylaxis.
The results also indicate a similar association between homocysteine and prevalent stroke among black and white adults.
A quantitative assessment of plasma homocysteine as a risk factor for vascular disease : probable benefits of increasing folic acid intakes.
The effects of folic acid and homocysteine are overlapping but distinct.
Although hyperhomocysteinaemia may cause ischaemic stroke, therapy aimed at lowering homocysteine level has shown only marginal benefits.
There are other mechanisms by which homocysteine may cause depression.
Adjusting for homocysteine levels marginally affected this relationship, but homocysteine did not emerge as a mediating factor.
Approximately 2-3% exists as free reduced homocysteine and the remaining unbound portion exists as mixed disulfides.
The investigators found that several cardiovascular risk factors are strongly associated with homocysteine concentrations, including age, systolic blood pressure and total cholesterol concentrations.
Nevertheless, the independence of folic acid and homocysteine in their relationship to depression is a noteworthy finding.
Sachdev et al. (pp. 529 -538) find that low serum folic acid and high homocysteine are correlates of depressive symptoms in community-dwelling middle-aged individuals.
One problem with the studies is that therapy may not have reduced homocysteine levels related to baseline levels or to control group levels enough to improve clinical outcome.
Genetic and nongenetic factors influencing plasma homocysteine levels in patients with ischemic cerebrovascular disease and in healthy control subjects.
Homocysteine and stroke were conducted in selected populations that did not reflect the age, gender, racial or ethnic distribution of the general population.
On the basis of current evidence, the case for the introduction of measuring the level of homocysteine in patients with ischaemic stroke into routine clinical practice is not supported.

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