1. Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer's Disease-Like Pathophysiology in APP/PS1 Mice.
- Author
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Fuchsberger T, Yuste R, Martinez-Bellver S, Blanco-Gandia MC, Torres-Cuevas I, Blasco-Serra A, Arango R, Miñarro J, Rodríguez-Arias M, Teruel-Marti V, Lloret A, and Viña J
- Subjects
- Administration, Oral, Alzheimer Disease genetics, Animals, Female, Flavoring Agents administration & dosage, Flavoring Agents toxicity, Male, Mice, Mice, Transgenic, Alzheimer Disease chemically induced, Alzheimer Disease pathology, Amyloid beta-Protein Precursor genetics, Presenilin-1 genetics, Sodium Glutamate administration & dosage, Sodium Glutamate toxicity
- Abstract
Glutamate excitotoxicity has long been related to Alzheimer's disease (AD) pathophysiology, and it has been shown to affect the major AD-related hallmarks, amyloid-β peptide (Aβ) accumulation and tau phosphorylation (p-tau). We investigated whether oral administration of monosodium glutamate (MSG) has effects in a murine model of AD, the double transgenic mice APP/PS1. We found that AD pathogenic factors appear earlier in APP/PS1 when supplemented with MSG, while wildtype mice were essentially not affected. Aβ and p-tau levels were increased in the hippocampus in young APP/PS1 animals upon MSG administration. This was correlated with increased Cdk5-p25 levels. Furthermore, in these mice, we observed a decrease in the AMPA receptor subunit GluA1 and they had impaired long-term potentiation. The Hebb-Williams Maze revealed that they had memory deficits. We show here for the first time that oral MSG supplementation can accelerate AD-like pathophysiology in a mouse model of AD.
- Published
- 2019
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