Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer's Disease

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Annotation Summary

Term Occurence Count Dictionary
cystinuria 1 endocrinologydiseases
folate deficiency 2 endocrinologydiseases
homocystinuria 1 endocrinologydiseases
hyperhomocysteinemia 6 endocrinologydiseases
vitamin B12 deficiency 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Select Disease Character Offset Disease Term Instance
cystinuria 29441 PolymorphismRelatively rare mutations of the gene encoding for CBS are frequently found in patients with homo cystinuria , but they do not seem to be more common in persons with moderately elevated plasma Hcy levels and were
folate deficiency 41498 balance, e.g., between DNA methylation and synthesis [[157]]. In addition, there is evidence that during folate deficiency , mechanisms are in place to preserve thymidylate and consequently DNA synthesis at the expense of Hcy
folate deficiency 43038 review see Fuso 2013 [[169]]). Evidence from transgenic mouse model of amyloid deposition shows that folate deficiency decreased SAM levels and DNA methyltransferase activity in the hippocampus and consequently increased
homocystinuria 29437 PolymorphismRelatively rare mutations of the gene encoding for CBS are frequently found in patients with homocystinuria , but they do not seem to be more common in persons with moderately elevated plasma Hcy levels and were
hyperhomocysteinemia 6908 compared to controls [[32]]. However, based on the available evidence, they could not establish that hyperhomocysteinemia preceded AD [[32]]. McCaddon and Miller [[35]] concluded that the available evidence showed a strong
hyperhomocysteinemia 14600 [[58],[59],[60],[61],[62],[63],[64],[65],[66],[67],[68]] and the mutation constitutes the most frequent cause of moderate hyperhomocysteinemia due to genetic factors [[20]]. There is some evidence for gender-specific differences: one study found
hyperhomocysteinemia 15838 levels in this genotype increased from 15 to 175 if plasma folate was ≤3.7 nmol/L [[73]]. Moreover, hyperhomocysteinemia in persons homozygous for the 677T mutation could be reversed or reduced with folic acid supplementation
hyperhomocysteinemia 18686 genotype is not completely clear: Vitamin B12 levels did not seem to have any effect on the risk of hyperhomocysteinemia in the 677TT genotype in some studies [[60],[71]], while others reported a negative association between
hyperhomocysteinemia 35883 mechanisms have been proposed for the link between elevated Hcy and AD and preclinical studies show that hyperhomocysteinemia , induced by genetic manipulation or by B-vitamin deficiency, causes known hallmarks of AD such as accumulation
hyperhomocysteinemia 39742 consequently been proposed that folate requirements might be increased due to irreversible oxidation and that hyperhomocysteinemia might be a consequence of the pro-oxidative environment and not just a result of inadequate intakes
vitamin B12 deficiency 24395 infarction [[94]]. It has been proposed that in conditions of elevated oxidative stress, functional vitamin B12 deficiency arises as the recycling into its active form cannot keep up with the rate of its oxidation [[95]]. Consequently,
vitamin B12 deficiency 44705 levels increase due to mechanisms most likely unrelated to the OCM [[95]]. As a consequence, functional vitamin B12 deficiency can develop if the rate of oxidation surpasses its recycling [[95]]. This effect is likely more pronounced

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