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The in vivo investigation of kynurenic acid (KYNA) and its analogs is one of the recent exciting topics in pharmacology. In the current study we assessed the biological effects of these molecules on bdelloid rotifers (Philodina acuticornis and Adineta vaga) by monitoring changes in their survival and phenotypical characteristics. In addition to longitudinal (slowly changing) markers (survival, number of rotifers alive and body size index), some dynamic (quickly responding) ones (cellular reduction capacity and mastax contraction frequency) were measured as well. KYNA and its analogs increased longevity, reproduction and growth, whereas reduction capacity and energy-dependent muscular activity decreased conversely. We found that spermidine, a calorie restriction mimetic, exerted similar changes in the applied micro-invertebrates. This characterized systemic profile evoked by the above-mentioned compounds was named beneficial physiologic attenuation. In reference experiments, using a stimulator (cyclic adenosine monophosphate) and a toxin (sodium azide), all parameters changed in the same direction (positively or negatively, respectively), as expected. The currently described adaptive phenomenon in bdelloid rotifers may provide holistic perspectives in translational research.

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StatementIn our current work we investigated the neurodegeneration-related and well-known neurotoxic beta-amyloid aggregate as an attenuator of autocatabolism-based organ shrinkage in an invertebrate micro-in vivo system. AbstractInvestigation of human neurodegeneration-related aggregates of beta-amyloid 1-42 (Aβ42) on bdelloid rotifers is a novel interdisciplinary approach in life sciences. We reapplied an organ size-based in vivo monitoring system, exploring the autocatabolism-related alterations evoked by Aβ42, in a glucosesupplemented starvation model. The experientially easy-to-follow size reduction of the bilateral reproductive organ (germovitellaria) in fasted rotifers was rescued by Aβ42, serving as a nutrient sourceand peptide sequence-specific attenuator of the organ shrinkage phase and enhancer of the regenerative one including egg reproduction. Recovery of the germovitellaria was significant in comparison with the greatly shrunken form. In contrast to the well-known neurotoxic Aβ42 (except the bdelloids) with specific regulatory roles, the artificially designed scrambled version (random order of amino acids) was inefficient in autocatabolism attenuation, behaving as negative control. This native Aβ42-related modulation of the 'functionally reversible organ shrinkage' can be a potential experiential and supramolecular marker of autocatabolism in vivo.

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