The fate of cell to cell transfer via tunnelling nanotubes in astroglia upon alpha synuclein protofibril treatment

Pathogenic aggregates of a-SYN can release from degenerating neurons, which can be taken up by surrounding neurons and glial cells. Neurodegenerative proteins induce biogenesis of f-actin-based intercellular membrane nanotubes (TNTs) and these TNTs facilitate inter-cellular transfer of prion proteins, viruses and cell organelles. Recent study from our lab reported, FAK-mediated regulation of Rho-associated kinases plays a significant role in actin membrane modulation, the biogenesis of TNTs, and successively proliferation. TNT-mediated cell-to-cell transfer not only accelerated degradation of a-SYN protofibrils, but helped cells to eliminate toxic dysfunctional mitochondria and curb ROS levels. In this study we observed the transfer of mitochondria through tunneling nanotubes and the fate in the transcription level expression. We hypothesize that the increase in ROS may induce the transfer of defective mitochondria and their clearance in the acceptor glial cells. Overall design: The experimental setup involved treating U-87 MG, alpha-synuclein protofibrils at 1 µM, 37°C, 5% CO2 for durations of 3, and 24 hours. Control is without the addition of alpha-synuclein protofibrils .