Affiliations: [a] Department NESMOS, Azienda Ospedaliera Sant'Andrea, “Sapienza” University of Rome, Rome, Italy | [b] Department of Surgery “Pietro Valdoni”, “Sapienza” University, Rome, Italy | [c] Center for Research in Neurobiology “Daniel Bovet”, “Sapienza” University, Rome, Italy | [d] Department of Psychology, Section of Neuroscience, “Sapienza” University, Rome, Italy
Correspondence:
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Correspondence to: Sigfrido Scarpa, Via A. Scarpa, 14, 00161 Roma, Italy. Tel.: +39 0649766600; Fax: +39 0649766600; E-mail: [email protected].
Note: [1] These authors equally contribute to this work.
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.
