Is L-methionine a trigger factor for Alzheimer's-like neurodegeneration?: Changes in Aβ oligomers, tau phosphorylation, synaptic proteins, Wnt signaling and behavioral impairment in wild-type mice. Issue 1 (December 2015)

• Record Type: Journal Article
• Authors: Tapia-Rojas, Cheril; Lindsay, Carolina; Montecinos-Oliva, Carla; Arrazola, Macarena; Retamales, Rocio; Bunout, Daniel; Hirsch, Sandra; Inestrosa, Nibaldo
• Is Part Of: Molecular neurodegeneration. Volume 10:Issue 1(2015)
• Page Start: 1
• Page End: 17
• Publication Date: 2015-12
• Subjects: L-Methionine -- Amyloid -- Tau -- Memory impairment -- Alzheimer's disease; Neurobiology -- Periodicals; Nervous system -- Diseases -- Periodicals; 616.8
• DOI: 10.1186/s13024-015-0057-0
• Languages: English
• ISSNs: 1750-1326

Abstract

Abstract Background L-methionine, the principal sulfur-containing amino acid in proteins, plays critical roles in cell physiology as an antioxidant and in the breakdown of fats and heavy metals. Previous studies suggesting the use of L-methionine as a treatment for depression and other diseases indicate that it might also improve memory and propose a role in brain function. However, some evidence indicates that an excess of methionine can be harmful and can increase the risk of developing Type-2 diabetes, heart diseases, certain types of cancer, brain alterations such as schizophrenia, and memory impairment. Results Here, we report the effects of an L-methionine-enriched diet in wild-type mice and emphasize changes in brain structure and function. The animals in our studypresented 1) higher levels of phosphorylatedtau protein, 2) increased levels of amyloid-β (Aβ)-peptides, including the formation of Aβ oligomers, 3) increased levels of inflammatory response, 4) increased oxidative stress, 5) decreased level of synaptic proteins, and 6) memory impairment and loss. We also observed dysfunction of theWnt signaling pathway. Conclusion Taken together, the results of our study indicate that an L-methionine-enriched diet causes neurotoxic effectsin vivo and might contribute to the appearance of Alzheimer's-like neurodegeneration.