Magnesium-L-threonate treats Alzheimer's disease by modulating the microbiota-gut-brain axis
Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer's disease model mice. However, the effects of magnesium-L-threonate...
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| Abstract | Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer's disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer's disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer's disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter. We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer's disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer's disease. |
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| AbstractList | Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer’s disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer’s disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer’s disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer’s disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter. We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer’s disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer’s disease. JOURNAL/nrgr/04.03/01300535-202410000-00029/figure1/v/2024-02-06T055622Z/r/image-tiff Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer's disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer's disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer's disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter. We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer's disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer's disease.JOURNAL/nrgr/04.03/01300535-202410000-00029/figure1/v/2024-02-06T055622Z/r/image-tiff Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer's disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer's disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer's disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter. We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer's disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer's disease. JOURNAL/nrgr/04.03/01300535-202410000-00029/figure1/v/2024-02-06T055622Z/r/image-tiff Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer's disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer's disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer's disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter. We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer's disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer's disease. JOURNAL/nrgr/04.03/01300535-202410000-00029/figure1/v/2025-03-16T123217Z/r/image-tiff Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer’s disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer’s disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer’s disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer’s disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter . We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer’s disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer’s disease. Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer’s disease. Magnesium-L-threonate has recently been found to have protective effects on learning and memory in aged and Alzheimer’s disease model mice. However, the effects of magnesium-L-threonate on the gut microbiota in Alzheimer’s disease remain unknown. Previously, we reported that magnesium-L-threonate treatment improved cognition and reduced oxidative stress and inflammation in a double-transgenic line of Alzheimer’s disease model mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1). Here, we performed 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry to analyze changes in the microbiome and serum metabolome following magnesium-L-threonate exposure in a similar mouse model. Magnesium-L-threonate modulated the abundance of three genera in the gut microbiota, decreasing Allobaculum and increasing Bifidobacterium and Turicibacter . We also found that differential metabolites in the magnesium-L-threonate-regulated serum were enriched in various pathways associated with neurodegenerative diseases. The western blotting detection on intestinal tight junction proteins (zona occludens 1, occludin, and claudin-5) showed that magnesium-L-threonate repaired the intestinal barrier dysfunction of APP/PS1 mice. These findings suggest that magnesium-L-threonate may reduce the clinical manifestations of Alzheimer’s disease through the microbiota-gut-brain axis in model mice, providing an experimental basis for the clinical treatment of Alzheimer’s disease. |
| Author | Liao, Wang Wei, Jiana Ruan, Yuting Zhou, Xianju Cao, Zhiyu Sheng, Zonghai Luo, Haoyu Xu, Jiaxin Zheng, Dong Yu, Qun Liu, Chongxu Mai, Yingren Liu, Jun |
| AuthorAffiliation | Department of Neurology,The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China%Department of Neurology,The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China;Special Medical Service Center,Neuroscience Center,Integrated Hospital of Traditional Chinese Medicine,Southern Medical University,Guangdong,Guangdong Province,China%Department of Rehabilitation,The Second Affiliated Hospital,Guangzhou Medical University,Guangzhou,Guangdong Province,China%Department of Neurology,Sun Yat-sen Memorial Hospital,Sun Yat-sen University,Guangzhou,Guangdong Province,China%Department of Neurology,The Affiliated Brain Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China%Institute of Biomedical and Health Engineering,Shenzhen Institute of Advanced Technology,Chinese Academy of Sciences,Shenzhen,Guangdong Province,China%Special Medical Service Center,Neuroscience Center,Integrated Hospital of Traditio |
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| Author_xml | – sequence: 1 givenname: Wang surname: Liao fullname: Liao, Wang – sequence: 2 givenname: Jiana surname: Wei fullname: Wei, Jiana – sequence: 3 givenname: Chongxu surname: Liu fullname: Liu, Chongxu – sequence: 4 givenname: Haoyu surname: Luo fullname: Luo, Haoyu – sequence: 5 givenname: Yuting surname: Ruan fullname: Ruan, Yuting – sequence: 6 givenname: Yingren surname: Mai fullname: Mai, Yingren – sequence: 7 givenname: Qun surname: Yu fullname: Yu, Qun – sequence: 8 givenname: Zhiyu surname: Cao fullname: Cao, Zhiyu – sequence: 9 givenname: Jiaxin surname: Xu fullname: Xu, Jiaxin – sequence: 10 givenname: Dong surname: Zheng fullname: Zheng, Dong – sequence: 11 givenname: Zonghai surname: Sheng fullname: Sheng, Zonghai – sequence: 12 givenname: Xianju orcidid: 0000-0003-1744-556X surname: Zhou fullname: Zhou, Xianju – sequence: 13 givenname: Jun orcidid: 0000-0003-0526-3523 surname: Liu fullname: Liu, Jun |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38488562$$D View this record in MEDLINE/PubMed |
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| Keywords | serum metabolites magnesium-L-threonate inflammation microbiota-gut-brain axis APP/PS1 double-transgenic Alzheimer's disease mouse model intestinal barrier dysfunction Alzheimer's disease microbiome oxidative stress |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this paper. Author contributions: Study design: XZ, JL; implementation of experiments: WL, JW, CL; data collection: HL, YR, YM; data analysis: QY, ZC, JX, DZ, ZS; manuscript draft: WL, JW, CL, XZ, JL. All authors have read and approved the final manuscript. |
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| Publisher | Wolters Kluwer - Medknow Medknow Publications & Media Pvt. Ltd Special Medical Service Center,Neuroscience Center,Integrated Hospital of Traditional Chinese Medicine,Southern Medical University,Guangdong,Guangdong Province,China%Department of Rehabilitation,The Second Affiliated Hospital,Guangzhou Medical University,Guangzhou,Guangdong Province,China%Department of Neurology,Sun Yat-sen Memorial Hospital,Sun Yat-sen University,Guangzhou,Guangdong Province,China%Department of Neurology,The Affiliated Brain Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China%Institute of Biomedical and Health Engineering,Shenzhen Institute of Advanced Technology,Chinese Academy of Sciences,Shenzhen,Guangdong Province,China%Special Medical Service Center,Neuroscience Center,Integrated Hospital of Traditional Chinese Medicine,Southern Medical University,Guangdong,Guangdong Province,China Department of Neurology,The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China%Department of Neurology,The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou,Guangdong Province,China Wolters Kluwer Medknow Publications |
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| SubjectTerms | Alzheimer's disease alzheimer’s disease; app/ps1 double-transgenic alzheimer’s disease mouse model; inflammation; intestinal barrier dysfunction; magnesium-l-threonate; microbiome; microbiota-gut-brain axis; oxidative stress; serum metabolites Disease Gut-brain axis Microbiota Research Article |
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| Title | Magnesium-L-threonate treats Alzheimer's disease by modulating the microbiota-gut-brain axis |
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