Oxidative stress, protein modification and Alzheimer disease

A. Tramutola, C. Lanzillotta, M. Perluigi, D. Allan Butterfield

Research output: Contribution to journalReview articlepeer-review

211 Scopus citations


Alzheimer disease (AD) is a progressive neurodegenerative disease that affects the elderly population with complex etiology. Many hypotheses have been proposed to explain different causes of AD, but the exact mechanisms remain unclear. In this review, we focus attention on the oxidative-stress hypothesis of neurodegeneration and we discuss redox proteomics approaches to analyze post-mortem human brain from AD brain. Collectively, these studies have provided valuable insights into the molecular mechanisms involved both in the pathogenesis and progression of AD, demonstrating the impairment of numerous cellular processes such as energy production, cellular structure, signal transduction, synaptic function, mitochondrial function, cell cycle progression, and degradative systems. Each of these cellular functions normally contributes to maintain healthy neuronal homeostasis, so the deregulation of one or more of these functions could contribute to the pathology and clinical presentation of AD. In particular, we discuss the evidence demonstrating the oxidation/dysfunction of a number of enzymes specifically involved in energy metabolism that support the view that reduced glucose metabolism and loss of ATP are crucial events triggering neurodegeneration and progression of AD.

Original languageEnglish
Pages (from-to)88-96
Number of pages9
JournalBrain Research Bulletin
StatePublished - Jul 2017

Bibliographical note

Publisher Copyright:
© 2016 Elsevier Inc.


  • ATP synthase
  • Alzheimer disease
  • Glucose metabolism
  • Oxidative stress
  • Protein oxidation

ASJC Scopus subject areas

  • General Neuroscience


Dive into the research topics of 'Oxidative stress, protein modification and Alzheimer disease'. Together they form a unique fingerprint.

Cite this