Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in a micro-in vivo system

• DOI: 10.1016/j.ibror.2020.10.002
• Publication Date: 2020-10-06T15:39:51Z
• Authors: Evelin Balazs; Zita Galik-Olah; Bence Galik; Zsolt Bozso; Janos Kalman; Zsolt Datki
• Keywords: Attenuator (electronics); Amyloid (mycology)

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