Oxidation of potassium channels by ROS: a general mechanism of aging and neurodegeneration?

Federico Sesti, Shuang Liu, Shi Qing Cai

Research output: Contribution to journalReview articlepeer-review

94 Scopus citations

Abstract

A wealth of evidence underscores the tight link between oxidative stress, neurodegeneration and aging. When the level of excess reactive oxygen species (ROS) increases in the cell, a phenomenon characteristic of aging, DNA is damaged, proteins are oxidized, lipids are degraded and more ROS are produced, all culminating in significant cell injury. Recently we showed that in the nematode, Caenorhabditis elegans, oxidation of K+ channels by ROS is a major mechanism underlying the loss of neuronal function. The C. elegans results support an argument that K+ channels controlling neuronal excitability and survival might provide a common, functionally important substrate for ROS in aging mammals. Here we discuss the implications that oxidation of K+ channels by ROS might have for the mammalian brain during normal aging, as well as in neurodegenerative diseases such as Alzheimer's and Parkinson's. We argue that oxidation of K+ channels by ROS is a common theme in the aging brain and suggest directions for future experimentation.

Original languageEnglish (US)
Pages (from-to)45-51
Number of pages7
JournalTrends in Cell Biology
Volume20
Issue number1
DOIs
StatePublished - Jan 1 2010

All Science Journal Classification (ASJC) codes

  • Cell Biology

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