Iron A pathological mediator of Alzheimer disease?

Raj K. Rolston, George Perry, Xiongwei Zhu, Rudy J. Castellani, Barney E. Dwyer, Hyoung Gon Lee, Robert B. Petersen, Mark A. Smith

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Metal-catalyzed oxidation and free radical formation are potent mediators of cellular injury to every category of macromolecule found in vulnerable neuronal populations and are thought to play an early and central role in Alzheimer disease (AD) pathogenesis. While metal-binding sites are present in proteins that accumulate in AD, metal-associated redox activity is primarily noted with nucleic acids, specifically with cytoplasmic RNA. Iron dyshomeostasis in AD is thought to arise from haem breakdown and mitochondrial turnover, and a reduction in microtubule density in vulnerable neurons increases redox-active metals, initiating a cascade of events culminating in characteristic pathologic features. Increased understanding of these early changes may be translated into more effective therapeutic modalities for AD than those currently in use.

Original languageEnglish (US)
Pages (from-to)33-36
Number of pages4
JournalAgro Food Industry Hi-Tech
Volume19
Issue number6
StatePublished - Nov 2008
Externally publishedYes

ASJC Scopus subject areas

  • Food Science
  • Industrial and Manufacturing Engineering

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