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Betaine reduces betha-amyloid-induced paralysis through activation of cystathionine-betha-synthase in an Alzheimer model of Caenorhabditis elegans

Leiteritz, Anne ; Dilberger, Benjamin ; Wenzel, Uwe ; Fitzenberger, Elena


Originalveröffentlichung: (2018) Genes and Nutrition 13(1):21 doi: 10.1186/s12263-018-0611-9
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URN: urn:nbn:de:hebis:26-opus-145978
URL: http://geb.uni-giessen.de/geb/volltexte/2019/14597/

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Freie Schlagwörter (Englisch): Alzheimer’s disease, betha-Amyloid , Caenorhabditis elegans , Hyperhomocysteinemia , Betaine
Sammlung: Open Access - Publikationsfonds
Universität Justus-Liebig-Universität Gießen
Institut: Molecular Nutrition Research, Interdisciplinary Research Center
Fachgebiet: Haushalts- und Ernährungswissenschaften - Ökotrophologie
DDC-Sachgruppe: Haushaltswissenschaften
Dokumentart: Aufsatz
Sprache: Englisch
Erstellungsjahr: 2018
Publikationsdatum: 20.05.2019
Kurzfassung auf Englisch: Background: The neurodegenerative disorder Alzheimer´s disease is caused by the accumulation of toxic aggregates of betha-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 Caenorhabditis elegans strain CL2006, to test whether betaine is able to reduce betha-amyloid-induced paralysis in C. elegans. This model expresses human betha-amyloid 1-42 under control of a muscle-specific promoter that leads to progressive, age-dependent paralysis in the nematodes.
Results: Betaine 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-betha-synthase using RNA interference both increased homocysteine levels and paralysis. Additionally, it prevented the reducing effects of betaine on homocysteine levels and paralysis.
Conclusion: Our studies show that betaine is able to reduce homocysteine levels and betha-amyloid-induced toxicity in a C. elegans model for Alzheimer´s disease. This effect is independent of the remethylation pathway but requires the transsulfuration pathway mediated by cystathionine-betha-synthase.
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