Glutamine Supplementation Preserves Glutamatergic Neuronal Activity in the Infralimbic Cortex, Which Delays the Onset of Mild Cognitive Impairment in 3xTg-AD Female Miceopen access
- Authors
- Baek, Ji Hyeong; Kang, Jae Soon; Song, Miyoung; Lee, Dong Kun; Kim, Hyun Joon
- Issue Date
- Jun-2023
- Publisher
- MDPI
- Keywords
- mild cognitive impairment; 3xTg-AD; glutamine; glutamatergic neuronal activity; oxidative stress
- Citation
- NUTRIENTS, v.15, no.12
- Indexed
- SCIE
SCOPUS
- Journal Title
- NUTRIENTS
- Volume
- 15
- Number
- 12
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/67727
- DOI
- 10.3390/nu15122794
- ISSN
- 2072-6643
- Abstract
- 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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