Abstract Title:

Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer's Disease-Like Pathophysiology in APP/PS1 Mice.

Abstract Source:

J Alzheimers Dis. 2019 Oct 21. Epub 2019 Oct 21. PMID: 31658055

Abstract Author(s):

Tanja Fuchsberger, Raquel Yuste, Sergio Martinez-Bellver, Mari-Carmen Blanco-Gandia, Isabel Torres-Cuevas, Arantxa Blasco-Serra, Román Arango, Jose Miñarro, Marta Rodríguez-Arias, Vicent Teruel-Marti, Ana Lloret, Jose Viña

Article Affiliation:

Tanja Fuchsberger


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.

Study Type : Animal Study

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