4.7 Article

Glutamine Supplementation Preserves Glutamatergic Neuronal Activity in the Infralimbic Cortex, Which Delays the Onset of Mild Cognitive Impairment in 3xTg-AD Female Mice

Journal

NUTRIENTS
Volume 15, Issue 12, Pages -

Publisher

MDPI
DOI: 10.3390/nu15122794

Keywords

mild cognitive impairment; 3xTg-AD; glutamine; glutamatergic neuronal activity; oxidative stress

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It was found that glutamine supplementation can activate glutamatergic neurotransmission and prevent chronic-stress-induced mild cognitive impairment (MCI). This study evaluated the effects of glutamine on glutamatergic activity and cognitive impairment in a triple-transgenic Alzheimer's disease mouse model (3xTg-AD). The results showed that a glutamine-supplemented diet delayed the onset of MCI in the mouse model predisposed to cognitive impairment and dementia.
It was recently found that glutamine (Gln) supplementation activates glutamatergic neurotransmission and prevents chronic-stress-induced mild cognitive impairment (MCI). In this study, we evaluated the effects of Gln on glutamatergic activity in the medial prefrontal cortex and the onset of cognitive impairment in a triple-transgenic Alzheimer's disease mouse model (3xTg-AD). Female 3xTg-AD mice were fed a normal diet (3xTg) or a Gln-supplemented diet (3xTg+Gln) from 2 to 6 months of age. Glutamatergic neuronal activity was analyzed at 6 months, and cognitive function was examined at 2, 4, and 6 months. 3xTg mice exhibited a decrease in glutamatergic neurotransmission in the infralimbic cortex, but 3xTg+Gln mice did not. The 3xTg group showed MCI at 6 months of age, but the 3xTg+Gln group did not. The expressions of amyloid peptide, inducible nitric oxide synthase, and IBA-1 were not elevated in the infralimbic cortex in the 3xTg+Gln group. Therefore, a Gln-supplemented diet could delay the onset of MCI even in a mouse model predisposed to cognitive impairment and dementia through genetic modification.

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