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ABSTRACT
Computer-based analysis of motility was used as a measure of amyloid-β (Aβ) proteotoxicity in the transgenic strain GMC101, expressing human Aβ1-42 in body wall muscle cells. Aβ-aggregation was quantified to relate the effects of caprylic acid (CA) to the amount of the proteotoxic protein. Gene knockdowns were induced through RNA-interference (RNAi). Moreover, the estimation of adenosine triphosphate (ATP) levels, the mitochondrial membrane potential (MMP) and oxygen consumption served the evaluation of mitochondrial function. CA improved the motility of GMC101 nematodes and reduced Aβ aggregation. Whereas RNAi for orthologues encoding key enzymes for α-lipoic acid and ketone bodies synthesis did not affect motility stimulation by CA, knockdown of orthologues involved in β-oxidation of fatty acids diminished its effects. The efficient energy gain by application of CA was finally proven by the increase of ATP levels in association with increased oxygen consumption and MMP. In conclusion, CA attenuates Aβ proteotoxicity by supplying energy via FAO. Since especially glucose oxidation is disturbed in Alzheimer´s disease, CA could potentially serve as an alternative energy fuel.
Acknowledgements
The authors thank Michele Perni and the Center for Misfolding Diseases, Department of Chemistry, University of Cambridge for providing the WF-NTP.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data that support the findings of this study are available from the corresponding author, Wenzel U, upon reasonable request.
Additional information
Notes on contributors
Stefan Baumanns
Stefan Baumanns, M.Sc. nutritional science and Ph.D. student, works on the relevance of mitochondrial quality control and the proteostasis network in the context of Alzheimer’s disease using the nematode Caenorhabditis elegans as a model.
Fabian Schmitt
Fabian Schmitt, M.Sc. nutritional science and Ph.D. student, works on the importance of cofilin in the context of Alzheimer’s disease using the nematode Caenorhabditis elegans as a model.
Christopher Spahn
Christopher Spahn, master student of nutritional science, used the nematode Caenorhabditis elegans as a model of Alzheimer’s disease in his bachelor’s thesis.
Anne E. Ringelmann
Anne E. Ringelmann, master student of nutritional science, used the nematode Caenorhabditis elegans as a model of Alzheimer’s disease in her bachelor’s thesis.
Daniel M. Beis
Daniel M. Beis, Dr. rer. nat. and lab manager, supervises human trials investigating stress-induced eating behavior and coordinates research on Alzheimer’s disease using the nematode Caenorhabditis elegans.
Gunter P. Eckert
Gunter P. Eckert, professor of nutrition in prevention and therapy, publishes in the fields of aging, age-related diseases and the involvement of mitochondrial function using cellular models, animal models and the nematode Caenorhabditis elegans. Amongst his recent publications is: Effects of Urolithin A on Mitochondrial Parameters in a Cellular Model of Early Alzheimer Disease. Int J Mol Sci. (2021) 22(15):8333. doi: 10.3390/ijms22158333
Uwe Wenzel
Uwe Wenzel, professor of molecular nutrition research, publishes on the effects of polyphenols in the context of prevention of cellular degeneration in the nematode C. elegans. Amongst his recent publications is: The polyphenol quercetin protects from glucotoxicity depending on the aggresome in Caenorhabditis elegans. European Journal of Nutrition (2020) 59(2):485-91. doi: 10.1007/s00394-019-01917-6.