Protective effects of CCL01 against Aβ-induced neurotoxicity in 5xFAD transgenic mouse model of Alzheimer's disease DOI Open Access
In Gyoung Ju, Su Young Son, Seung-Min Lee

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 158, P. 114105 - 114105

Published: Dec. 9, 2022

Alzheimer's disease (AD) is the most common dementia characterized by excessive accumulation of amyloid-beta (Aβ) and tau aggregates, as well neuronal damage neuroinflammation. Metabolic disruption in AD has been noticed because metabolite alterations closely correlate with Aβ neuropathology behavioral phenotypes. Accordingly, controlling various neuropathological processes metabolic an efficient therapeutic strategy for treatment. In this study, we evaluated effects a combination Cuscuta seeds Lactobacillus paracasei NK112 (CCL01) on altered metabolism five familial (5xFAD) transgenic mice cell cultures. First, observed that CCL01 exerted neuroprotective HT22 hippocampal neurons primary cultured neurons. ameliorated memory decline protected synapses survival 5xFAD mice. These were related to inhibition phosphorylation. also inhibited activation mitogen-activated protein kinase (MAPK) signaling neuroinflammatory processes. Moreover, profile-particularly phospholipid metabolism-was significantly changed group, while partly restored alteration. Lysophosphatidylcholine (lysoPC), levels which higher brains mice, neurotoxicity vitro, whereas from lysoPC-induced toxicity regulating MAPK signaling. Additionally, administration reduced gut inflammation summary, demonstrated improved function protecting against Aβ- through regulation signaling, neuroinflammation, phosphorylation, inflammation, suggesting potential treatment AD.

Language: Английский

Protective effects of CCL01 against Aβ-induced neurotoxicity in 5xFAD transgenic mouse model of Alzheimer's disease DOI Open Access
In Gyoung Ju, Su Young Son, Seung-Min Lee

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 158, P. 114105 - 114105

Published: Dec. 9, 2022

Alzheimer's disease (AD) is the most common dementia characterized by excessive accumulation of amyloid-beta (Aβ) and tau aggregates, as well neuronal damage neuroinflammation. Metabolic disruption in AD has been noticed because metabolite alterations closely correlate with Aβ neuropathology behavioral phenotypes. Accordingly, controlling various neuropathological processes metabolic an efficient therapeutic strategy for treatment. In this study, we evaluated effects a combination Cuscuta seeds Lactobacillus paracasei NK112 (CCL01) on altered metabolism five familial (5xFAD) transgenic mice cell cultures. First, observed that CCL01 exerted neuroprotective HT22 hippocampal neurons primary cultured neurons. ameliorated memory decline protected synapses survival 5xFAD mice. These were related to inhibition phosphorylation. also inhibited activation mitogen-activated protein kinase (MAPK) signaling neuroinflammatory processes. Moreover, profile-particularly phospholipid metabolism-was significantly changed group, while partly restored alteration. Lysophosphatidylcholine (lysoPC), levels which higher brains mice, neurotoxicity vitro, whereas from lysoPC-induced toxicity regulating MAPK signaling. Additionally, administration reduced gut inflammation summary, demonstrated improved function protecting against Aβ- through regulation signaling, neuroinflammation, phosphorylation, inflammation, suggesting potential treatment AD.

Language: Английский

Citations

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