Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in amicro-in vivosystem

Abstract

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.

Translational biomedicine-oriented exploratory research on bioactive rotifer-specific biopolymers

“…The autocatabolism-attenuator effect of beta-amyloids in these animals also demonstrates such a case. 24 A similar interdisciplinary regulatory interaction is the effect of kynurenic acid on the metabolism of rotifers. 25 Several studies have proven that this ancient molecule alone prominently and adequately represents the multifunctionality occurring in nature or specific effects on the nervous system.…”