Systemic and central nervous system metabolic alterations in Alzheimer’s disease

Velpen, Vera van der; Teav, Tony; Gallart-Ayala, Héctor; Mehl, Florence; Konz, Ioana; Clark, Christopher; Oikonomidi, Aikaterini; Peyratout, Gwendoline; Henry, Hugues; Delorenzi, Mauro; Ivanišević, Julijana; Popp, Julius

doi:10.1186/s13195-019-0551-7

Cited by 174 publications

(172 citation statements)

References 54 publications

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“…The mRNA expression of BDNF and ciliary neurotrophic factor (CNTF) in PC12 cells was lower in the AD-Con group than the Normal-Con group, and the high dosage of TTK-E and TTK-W prevented the decrease in BDNF and CNTF by amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) (Figure 1B,C). TTK-E produced higher mRNA expression of BDNF and CNTF than TTK-W. A high dosage of TTK-E exhibited a similar mRNA expression of CNTF as the Normal-Con group (Figure 1B,C).…”

Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

“…Cell survival and expression of brain growth factors in the nerve growth factor-administered PC12 cells. The cells had treatments with 70% ethanol Tetragonia tetragonioides or its water extract with 10 and 50 µg/mL dosages, and after 1 h, cell death was induced by 10 µM amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). After 24 h treatment, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and mRNA expression were measured.…”

Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

“…After 24 h treatment, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and mRNA expression were measured. Amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) was administered without Tetragonia tetragonioides Kuntze (TTK) extract (AD-Con), ethanol extract (TTK-E), or water extract (TTK-W), and 10 µM amyloid-β was administered without TTK extract (Normal-Con). (A) Cell survival determined by MTT assay.…”

Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

“…(C) Frequencies to visit the zone where the platform was located, duration to stay in the zone, and the latency to visit the zone at first. AD and Non-AD rats infused amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) into the CA1 regions and amyloid-β into the CA1 regions, respectively. AD-Con fed 45% fat diet with 0.5% dextrin in AD rats infused intra-CA1 infusion of amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), AD-TTK fed 45% fat diet with 0.5% water extract of Tetragonia tetragonioides (TTK) in AD rats, and Normal-Con fed 45% fat diet with 0.5% dextrin in non-AD rats infused intra-CA1 infusion of amyloid-β .…”

Section: Amyloid-β Accumulation In the Hippocampusmentioning

confidence: 99%

“…The percentage of Bacteroidales and Lactobacillales decreased in the AD-Con compare to the Normal-Con, and the decrease was prevented by AD-TKK ( Figure 6D). fat diet with 0.5% dextrin in AD rats infused intra-CA1 infusion of amyloid-β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), AD-TTK fed 45% fat diet with 0.5% water extract of Tetragonia tetragonioides (TTK) in AD rats, and Normal-Con fed 45% fat diet with 0.5% dextrin in non-AD rats infused intra-CA1 infusion of amyloid-β . Each value represents the mean ± SD of five mice in each group.…”

Section: Gut Microbiomementioning

confidence: 99%

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Tetragonia tetragonioides Protected against Memory Dysfunction by Elevating Hippocampal Amyloid-β Deposition through Potentiating Insulin Signaling and Altering Gut Microbiome Composition

Kim

Ryuk

et al. 2020

IJMS

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Alzheimer's disease (AD) is a progressive neurodegenerative disease. Herbal medicine may provide efficacious treatments for its prevention and/or cure. This study investigated whether a 70% ethanol extract of Tetragonia tetragonioides Kuntze (TTK; New Zealand spinach) improved the memory deficit by reducing hippocampal amyloid-β deposition and modulating the gut microbiota in rats with amyloid-β(25-35) infused into the hippocampus (AD rats) in an AD animal model. The AD rats had cellulose (AD-CON) or TTK (300 mg/kg bw; AD-TTK) in their high-fat diets for seven weeks. Rats with amyloid-β(35-25) infused into the hippocampus fed an AD-Con diet did not have memory loss (Normal-Con). AD-TTK protected against amyloid-β deposition compared to AD-Con, but it was higher than Normal-Con. AD-TTK protected against short-term and special memory loss measured by passive avoidance, Y maze, and water maze, compared to AD-Con. Compared to the Normal-Con, AD-Con attenuated hippocampal pCREB → pAkt → pGSK-3β, which was prevented in the AD-TTK group. Brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) mRNA expression decreased in the AD-CON group, and their expression was prevented in the AD-TTK group. Hippocampal TNF-α and IL-1β mRNA expressions were higher in the AD-Con group than in the Normal-Con, and AD-TTK groups protected against the increase in their expression. The AD-CON group showed an increase in insulin resistance compared to the Normal-Con group and the AD-TTK group showed improvement. AD-Con separated the gut microbiome community compared to the Normal-Con group and AD-TTK overlapped with the normal-Con. The AD-Con group had more Clostridiales, Erysipelotrichales, and Desulfovibrionales than the AD-TKK and Normal-Con group but fewer Lactobacilales and Bacteroidales. In conclusion, the 70% ethanol extract of TTK enhanced the memory function and potentiated hippocampal insulin signaling, reduced insulin resistance, and improved gut microbiota in amyloid-β-infused rats.

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Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

Section: Ttk Extracts In Neural Cell Survival In Vitromentioning

confidence: 99%

Section: Amyloid-β Accumulation In the Hippocampusmentioning

confidence: 99%

Section: Gut Microbiomementioning

confidence: 99%

See 3 more Smart Citations

Tetragonia tetragonioides Protected against Memory Dysfunction by Elevating Hippocampal Amyloid-β Deposition through Potentiating Insulin Signaling and Altering Gut Microbiome Composition

Kim

Ryuk

et al. 2020

IJMS

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Exploring links between 2‐oxoglutarate‐dependent oxygenases and Alzheimer's disease

Liu

Xie

Wang

et al. 2022

Alzheimer's & Dementia

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Hypoxia, that is, an inadequate oxygen supply, is linked to neurodegeneration and patients with cardiovascular disease are prone to Alzheimer's disease (AD). 2‐Oxoglutarate and ferrous iron‐dependent oxygenases (2OGDD) play a key role in the regulation of oxygen homeostasis by acting as hypoxia sensors. 2OGDD also have roles in collagen biosynthesis, lipid metabolism, nucleic acid repair, and the regulation of transcription and translation. Many biological processes in which the >60 human 2OGDD are involved are altered in AD patient brains, raising the question as to whether 2OGDD are involved in the transition from normal aging to AD. Here we give an overview of human 2OGDD and critically discuss their potential roles in AD, highlighting possible relationships with synapse dysfunction/loss. 2OGDD may regulate neuronal/glial differentiation through enzyme activity‐dependent mechanisms and modulation of their activity has potential to protect against synapse loss. Work linking 2OGDD and AD is at an early stage, especially from a therapeutic perspective; we suggest integrated pathology and in vitro discovery research to explore their roles in AD is merited. We hope to help enable long‐term research on the roles of 2OGDD and, more generally, oxygen/hypoxia in AD. We also suggest shorter term empirically guided clinical studies concerning the exploration of 2OGDD/oxygen modulators to help maintain synaptic viability are of interest for AD treatment.

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Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases

Huseby

Delvaux

Brokaw

et al. 2022

Alzheimer's & Dementia

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Background Dysfunctional processes in Alzheimer's disease and other neurodegenerative diseases lead to neural degeneration in the central and peripheral nervous system. Research demonstrates that neurodegeneration of any kind is a systemic disease that may even begin outside of the region vulnerable to the disease. Neurodegenerative diseases are defined by the vulnerabilities and pathology occurring in the regions affected. Method A random forest machine learning analysis on whole blood transcriptomes from six neurodegenerative diseases generated unbiased disease‐classifying RNA transcripts subsequently subjected to pathway analysis. Results We report that transcripts of the blood transcriptome selected for each of the neurodegenerative diseases represent fundamental biological cell processes including transcription regulation, degranulation, immune response, protein synthesis, apoptosis, cytoskeletal components, ubiquitylation/proteasome, and mitochondrial complexes that are also affected in the brain and reveal common themes across six neurodegenerative diseases. Conclusion Neurodegenerative diseases share common dysfunctions in fundamental cellular processes. Identifying regional vulnerabilities will reveal unique disease mechanisms. Highlights Transcriptomics offer information about dysfunctional processes. Comparing multiple diseases will expose unique malfunctions within diseases. Blood RNA can be used ante mortem to track expression changes in neurodegenerative diseases. Protocol standardization will make public datasets compatible.

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Systemic and central nervous system metabolic alterations in Alzheimer’s disease

Cited by 174 publications

References 54 publications

Tetragonia tetragonioides Protected against Memory Dysfunction by Elevating Hippocampal Amyloid-β Deposition through Potentiating Insulin Signaling and Altering Gut Microbiome Composition

Tetragonia tetragonioides Protected against Memory Dysfunction by Elevating Hippocampal Amyloid-β Deposition through Potentiating Insulin Signaling and Altering Gut Microbiome Composition

Exploring links between 2‐oxoglutarate‐dependent oxygenases and Alzheimer's disease

Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases

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