Betaine reduces betha-amyloid-induced paralysis through activation of cystathionine-betha-synthase in an Alzheimer model of Caenorhabditis elegans
dc.contributor.author | Leiteritz, Anne | |
dc.contributor.author | Dilberger, Benjamin | |
dc.contributor.author | Wenzel, Uwe | |
dc.contributor.author | Fitzenberger, Elena | |
dc.date.accessioned | 2022-11-18T09:53:24Z | |
dc.date.available | 2019-05-20T09:17:20Z | |
dc.date.available | 2022-11-18T09:53:24Z | |
dc.date.issued | 2018 | |
dc.description.abstract | 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. | en |
dc.identifier.uri | http://nbn-resolving.de/urn:nbn:de:hebis:26-opus-145978 | |
dc.identifier.uri | https://jlupub.ub.uni-giessen.de//handle/jlupub/9432 | |
dc.identifier.uri | http://dx.doi.org/10.22029/jlupub-8820 | |
dc.language.iso | en | de_DE |
dc.rights | Namensnennung 4.0 International | * |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | Alzheimer s disease | en |
dc.subject | betha-Amyloid | en |
dc.subject | Caenorhabditis elegans | en |
dc.subject | Hyperhomocysteinemia | en |
dc.subject | Betaine | en |
dc.subject.ddc | ddc:640 | de_DE |
dc.title | Betaine reduces betha-amyloid-induced paralysis through activation of cystathionine-betha-synthase in an Alzheimer model of Caenorhabditis elegans | en |
dc.type | article | de_DE |
local.affiliation | FB 09 - Agrarwissenschaften, Ökotrophologie und Umweltmanagement | de_DE |
local.opus.fachgebiet | Haushalts- und Ernährungswissenschaften - Ökotrophologie | de_DE |
local.opus.id | 14597 | |
local.opus.institute | Molecular Nutrition Research, Interdisciplinary Research Center | de_DE |
local.source.freetext | Genes and Nutrition 13(1):21 | de_DE |
local.source.uri | https://doi.org/10.1186/s12263-018-0611-9 |
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