AI Article Synopsis
- - Late Onset Alzheimer's Disease (LOAD) is linked to high homocysteine levels and issues with one-carbon metabolism, which can be affected by B vitamin deficiency.
- - A study using TgCRND8 mice showed that B vitamin deficiency leads to changes in brain protein expression related to neuronal plasticity and mitochondrial functions, aligning with Alzheimer's disease characteristics such as increased amyloid-β plaques and oxidative stress.
- - The research suggests that the identified proteins could serve as new potential biomarkers for LOAD, indicating further areas for investigation in understanding the disease.
Article Abstract
Late Onset Alzheimer's Disease (LOAD) can be associated to high homocysteine level and alteration of one-carbon metabolism. We previously demonstrated in the TgCRND8 mice strain, over-expressing human amyloid-β protein precursor, that B vitamin deficiency causes alteration of one-carbon metabolism, together with unbalance of S-adenosylmethionine/S-adenosylhomocysteine levels, and is associated with AD like hallmarks as increased amyloid-β plaque deposition, hyperhomocysteinemia, and oxidative stress. The same model of nutritional deficit was used here to study the variation of the brain protein expression profile associated to B vitamin deficiency. A group of proteins mainly involved in neuronal plasticity and mitochondrial functions was identified as modulated by one-carbon metabolism. These findings are consistent with increasing data about the pivotal role of mitochondrial abnormalities in AD patho-physiology. The identified proteins might represent new potential biomarkers of LOAD to be further investigated.
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