Proteostasis and Nutrition in Neural Functions and Neurodegeneration

The concept for this Research Topic emerged from discussions held after the Deep Dive webinar dedicated to the Frontiers in Science lead article, Evolving surgical teams in the age of artificial intelligence and robotics.Proteostasis is one of the essential homeostatic systems, and is maintained with proper nutrition for physiological neural function. In this Research Topic, we aim to shed light on the relationship between proteostasis and nutrition for neural function and neurodegeneration, and to highlight the forefront of therapeutic development targeting these proteostatic pathways and nutritional interventions.Proteostasis, regulated by gene expression, translation, post-translational modification, protein folding, and protein degradation, is disrupted in a range of acute and chronic neurodegenerative disorders. Failure of the ubiquitin-proteasome system and autophagy, in particular, drives severe neurodegenerative diseases including Alzheimer’s Disease, Parkinson’s Disease, Prion Disease, Amyotrophic Lateral Sclerosis, and Spinocerebellar Ataxia, in which disease-responsible proteins unfold and transform into stable, degradation-resistant amyloid aggregates that induce toxic inflammation and severe damage in the nervous system.Nutrition plays a pivotal role in this process. Lack of essential amino acids inhibits protein synthesis and induces the unfolded protein response (UPR); vitamin B6 regulates amino acid metabolism and thus protein synthesis and UPR; low glucose depletes cellular energy and increases ROS production, driving protein degradation and apoptosis; vitamin B1 deficiency causes acute neuronal degeneration; and excess saturated fatty acids destabilize membrane proteins, further driving UPR and protein degradation.The relationship between proteinopathies and malnutrition-driven UPR is just emerging and largely remains to be explored: unfolded proteins and amyloids may induce chronic UPR, while malnutrition itself may induce protein unfolding and UPR in neural cells, in turn contributing to abnormal protein aggregation in the brain.This Research Topic welcomes contributions addressing:• Mechanisms of unfolded protein response (UPR) and protein misfolding in Alzheimer’s Disease, Parkinson’s Disease, Prion Disease, ALS, and Spinocerebellar Ataxia• The role of the ubiquitin-proteasome system and autophagy in proteostatic failure and neurodegeneration• The influence of amino acid, vitamin (B6, B1), glucose, and fatty acid status on neural proteostasis and UPR• Malnutrition-driven UPR as a contributor to abnormal protein aggregation in the brain• Therapeutic development targeting proteostatic pathways and nutritional interventionsWe encourage submissions of original research articles, reviews, mini-reviews, perspectives, and opinion pieces to contribute to this comprehensive exploration of nutritional proteostasis and novel therapeutic strategies. Topic editors: Hiroyuki Aizawa, Keiichi Kadoyama Source: https://www.frontiersin.org/research-topics/85215/proteostasis-and-nutrition-in-neural-functions-and-neurodegeneration