ArticleGenes & nutrition2018
Betaine reduces β-amyloid-induced paralysis through activation of cystathionine-β-synthase in an Alzheimer model of
Article in Genes & nutrition, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Exercise-mimicking effects of betaine in chronic disease prevention and management.Frontiers in nutrition · 2025Review
- A New Perspective for the Treatment of Alzheimer's Disease: Exosome-like Liposomes to Deliver Natural Compounds and RNA Therapies.Molecules (Basel, Switzerland) · 2023Review
- Betaine Mitigates Amyloid-β-Associated Neuroinflammation by Suppressing the NLRP3 and NF-κB Signaling Pathways in Microglial Cells.Journal of Alzheimer's disease : JAD · 2023Article
- Exploring the complexities of 1C metabolism: implications in aging and neurodegenerative diseases.Frontiers in aging neuroscience · 2023Review
- Effects of Combining Biofactors on Bioenergetic Parameters, Aβ Levels and Survival in Alzheimer Model Organisms.International journal of molecular sciences · 2022Article
- Alzheimer's Disease and Toxins Produced by Marine Dinoflagellates: An Issue to Explore.Marine drugs · 2022Review
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Review
- AFrontiers in microbiology · 2022Article
- Betaine-rich sugar beet molasses protects from homocysteine-induced reduction of survival in Caenorhabditis elegans.European journal of nutrition · 2020Article
- Betaine attenuates oxidative stress and cognitive dysfunction in an amyloid β-induced rat model of Alzheimer's disease.Research in pharmaceutical sciencesArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe neurodegenerative disorder Alzheimer's disease is caused by the accumulation of toxic aggregates of β-amyloid in the human brain. On the one hand, hyperhomocysteinemia has been shown to be a risk factor for cognitive decline in Alzheimer's disease. On the other hand, betaine has been demonstrated to attenuate Alzheimer-like pathological changes induced by homocysteine. It is reasonable to conclude that this is due to triggering the remethylation pathway mediated by betaine-homocysteine-methyltransferase. In the present study, we used the transgenic
resultsBetaine at a concentration of 100 μM was able to reduce homocysteine levels in the presence and absence of 1 mM homocysteine. Simultaneously, betaine both reduced normal paralysis rates in the absence of homocysteine and increased paralysis rates triggered by addition of homocysteine. Knockdown of cystathionine-β-synthase using RNA interference both increased homocysteine levels and paralysis. Additionally, it prevented the reducing effects of betaine on homocysteine levels and paralysis.
conclusionOur studies show that betaine is able to reduce homocysteine levels and β-amyloid-induced toxicity in a
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.