Clinical implications from proteomic studies in neurodegenerative diseases: Lessons from mitochondrial proteins

D. Allan Butterfield, Erika M. Palmieri, Alessandra Castegna

Research output: Contribution to journalReview articlepeer-review

21 Scopus citations

Abstract

Mitochondria play a key role in eukaryotic cells, being mediators of energy, biosynthetic and regulatory requirements of these cells. Emerging proteomics techniques have allowed scientists to obtain the differentially expressed proteome or the proteomic redox status in mitochondria. This has unmasked the diversity of proteins with respect to subcellular location, expression and interactions. Mitochondria have become a research hot spot in subcellular proteomics, leading to identification of candidate clinical targets in neurodegenerative diseases in which mitochondria are known to play pathological roles. The extensive efforts to rapidly obtain differentially expressed proteomes and unravel the redox proteomic status in mitochondria have yielded clinical insights into the neuropathological mechanisms of disease, identification of disease early stage and evaluation of disease progression. Although current technical limitations hamper full exploitation of the mitochondrial proteome in neurosciences, future advances are predicted to provide identification of specific therapeutic targets for neurodegenerative disorders.

Original languageEnglish
Pages (from-to)259-274
Number of pages16
JournalExpert Review of Proteomics
Volume13
Issue number3
DOIs
StatePublished - Mar 3 2016

Bibliographical note

Publisher Copyright:
© 2016 Taylor and Francis.

Keywords

  • Alzheimer disease
  • Parkinson disease
  • Proteomics
  • clinical biomarkers
  • mitochondria
  • neurodegeneration
  • redox proteomics

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Fingerprint

Dive into the research topics of 'Clinical implications from proteomic studies in neurodegenerative diseases: Lessons from mitochondrial proteins'. Together they form a unique fingerprint.

Cite this