Folate (Vitamin B9) 图表
6 来自同行评审研究的图表
Brain imaging studies demonstrate that elevated homocysteine is associated with accelerated rates of brain atrophy, particularly in medial temporal lobe structures critical for memory. B-vitamin treatment appears to slow this atrophy in individuals with elevated baseline homocysteine.
Homocysteine and Dementia: An International Consensus Statement.
A causal model illustrates how elevated plasma homocysteine may contribute to dementia through multiple pathways, interacting with other risk factors such as age, hypercholesterolemia, and genetic predisposition. No single factor is sufficient alone; rather, combinations of component causes drive disease.
Homocysteine and Dementia: An International Consensus Statement.
Meta-analyses of cohort studies consistently indicate that elevated homocysteine is associated with approximately doubled risk of Alzheimer's disease. The strength of this association persists after adjustment for common confounders including age, sex, and education.
Homocysteine and Dementia: An International Consensus Statement.
Moderate hyperhomocysteinemia resulting from low folate status is an independent risk factor for cardiovascular disease, dementia, and depression. This figure maps the clinical consequences of impaired folate metabolism due to genetic variants.
Genetic polymorphisms and folate status.
Population-level variation in folate-related genetic polymorphisms influences disease susceptibility across ethnic groups. This figure compares allele frequencies and associated health outcomes for key folate metabolism gene variants.
Genetic polymorphisms and folate status.
One-carbon metabolism pathways involving folate, vitamin B12, and vitamin B6 are mapped, showing key enzymatic reactions catalyzed by MTHFR and the roles of FAD and FMN as cofactors in homocysteine recycling.
Causes, Consequences and Public Health Implications of Low B-Vitamin Status in Ageing.