Abeta, oxidative stress in Alzheimer disease: evidence based on proteomics studies.

Abstract

The initiation and progression of Alzheimer disease (AD) is a complex process not yet fully understood. While many hypotheses have been provided as to the cause of the disease, the exact mechanisms remain elusive and difficult to verify. Proteomic applications in disease models of AD have provided valuable insights into the molecular basis of this disorder, demonstrating that on a protein level, disease progression impacts numerous cellular processes such as energy production, cellular structure, signal transduction, synaptic function, mitochondrial function, cell cycle progression, and proteasome function. Each of these cellular functions contributes to the overall health of the cell, and the dysregulation of one or more could contribute to the pathology and clinical presentation in AD. In this review, foci reside primarily on the amyloid β-peptide (Aβ) induced oxidative stress hypothesis and the proteomic studies that have been conducted by our laboratory and others that contribute to the overall understanding of this devastating neurodegenerative disease.

• Authors: Aaron M Swomley, Sarah Förster, Jierel T Keeney, Judy Triplett, Zhaoshu Zhang, Rukhsana Sultana, D Allan Butterfield
• Journal: Biochimica et biophysica acta (Biochim Biophys Acta) Vol. 1842 Issue 8 Pg. 1248-57 (Aug 2014) ISSN: 0006-3002 [Print] Netherlands
• PMID: 24120836 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
• Copyright: © 2013.

Chemical References

• Amyloid beta-Peptides
• Antioxidants

Topics

• Alzheimer Disease (metabolism, pathology)
• Amyloid beta-Peptides (metabolism)
• Animals
• Antioxidants (metabolism)
• Disease Models, Animal
• Humans
• Oxidative Stress
• Proteomics