doi: 10.3389/fendo.2023.1234824 355 SinghJSharmaMJainNAftabIVikramNSinghTPet al
Acknowledgements We thank J.E
As a result, neuronal toxicity from oxidative stress is amplified, leading finally to apoptosis.[9,12,37] The increased content of oxygen radicals due to high Hcy levels can also lead to hydrolysis of the precursor protein amyloid, increased generation of the -amyloid peptide, and formation of amyloid plaques in the neurons (one of the main characteristics of Alzheimer disease).[8,32] Independent of high Hcy levels, folic acid and vitamin B-12 also contribute to cognitive function.[1416] Folate deficiency affects nuclear and mitochondrial DNA synthesis due to lack of methylation of purines, and impedes transformation of uracil into thymine, causing oxidative stress and generation of reactive oxygen species, followed by neuronal deterioration and cellular death in areas of the brain involved in AD.[14,15] Folate deficiency can also cause hypomethylation of regions that modulate expression of genes presumably involved in AD pathogenesis.[14,15] In addition, vitamin B-12 is a cofactor of the enzyme methylmalonyl-CoA mutase
Patients were included if they had either participated in the WILD program for at least 6 months with a minimum of 2 visits or if they had achieved 10% body weight loss goal prior to the 6-month mark
