The Non-Cellular Autonomic Mechanism of Neuronal Degeneration: Protein Synthesis and Secretion

Dear Colleagues,

Unfolded protein response (UPR) is a physiological pathway that helps cells to survive in stress conditions. UPR involves three branches in the endoplasmic reticulum: the PERK, IRE1, and ATF6 pathways, leading to protein synthesis reduction, and the activation of protein degradation and chaperone gene transcription. Over activation of URP is associated with many neurodegenerative diseases, such as prion, Parkinson’s, and Alzheimer’s diseases. By blocking this mechanism, you can have a delay in the onset of the pathology, an improvement in behavioral test performance, and neuronal survival in animal models. UPR can spread from one cell to another, leading to a non-cell-autonomous mechanism of neuronal degeneration, which is reasonably ascribed to secreted factors.

In this Special Issue of Life, we want to invite researchers to share their new results and ideas related to UPR in non-neuronal cells involved in neuronal degeneration in the central nervous system (CNS), the alteration of secretion capacity, such as proteins or metabolites, and the transmission and impact of these on other cells.

Dr. Laura Tapella
Dr. Elena Restelli
Dr. Erica Buoso
Guest Editors

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