AI Article Synopsis
- Computer-based analysis assessed motility in transgenic GMC101 nematodes expressing human amyloid-β (Aβ) to evaluate the impact of caprylic acid (CA) on proteotoxicity and Aβ aggregation.
- CA enhanced nematode motility and reduced Aβ aggregation, with gene knockdowns showing that β-oxidation of fatty acids is critical for CA's effectiveness, while other metabolic pathways were not as affected.
- The positive effects of CA were linked to improved mitochondrial function, highlighting its potential as an alternative energy source in conditions like Alzheimer’s disease where glucose metabolism is impaired.
Article Abstract
Computer-based analysis of motility was used as a measure of amyloid-β (Aβ) proteotoxicity in the transgenic strain GMC101, expressing human Aβ 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.
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| http://dx.doi.org/10.1080/1028415X.2023.2180870 | DOI Listing |
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