An update on the interactions between Alzheimer's disease, autophagy and inflammation.

Gene

Department of Physiology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey. Electronic address:

Published: July 2019

AI Article Synopsis

  • This document discusses the relationship between inflammation and autophagy in the progression of Alzheimer's disease, highlighting how both factors contribute to the accumulation of misfolded proteins in the brain.
  • It emphasizes that inflammatory mediators can hinder the brain's ability to clear these harmful proteins, which is a key factor in developing Alzheimer's.
  • The text also outlines important areas for future research, particularly regarding how different inflammatory signals might impact the functioning of autophagy at a molecular level.

Article Abstract

An update on pathogenesis of Alzheimer's disease, the present document describes the crosstalk between autophagy and inflammation in Alzheimer's disease progression by assessing key findings and identifying gaps in the current knowledge. Inflammation mediators can disrupt the clearance of misfolded proteins. It is well defined that misfolded protein accumulation and aberrant level of inflammatory mediators in the brain can trigger Alzheimer's disease. Studies indicated that restoring the inflammatory and autophagy mediators improves Alzheimer's disease. This presents a problem: How inflammation interacts with the protein clearance system, autophagy, in the brain. Here, we describe an update on the link between inflammation and autophagy pathways. Some of the vital challenges for the presented link included investigation of the questions: What is the role of inflammation mediators in the brain under various conditions; and how altered level of inflammatory mediators affects the performance of autophagy at molecular level.

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Source
http://dx.doi.org/10.1016/j.gene.2019.04.040DOI Listing

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