Role of mitochondrial-mediated signaling pathways in Alzheimer disease and hypoxia

Cristina Carvalho, Sonia C Correia, Renato X Santos, Susana Cardoso, Paula I Moreira, Timothy A Clark, Xiongwei Zhu, Mark A Smith, George Perry (Corresponding Author)

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Development of effective treatments for Alzheimer’s disease is complicated by the poor understanding of its pathophysiology. Recent work suggests mitochondria may play a primary role in neurodegeneration, due to alterations in mitochondria turnover and that the brain is specifically susceptible, due to high energy demand. Mitochondria are the major source of cellular energy through oxidative phosphorylation and regulate intracellular calcium levels and survival pathways. Hypoxia has been implicated in several neurodegenerative diseases including Alzheimer’s disease. During hypoxic events, mitochondrial complex III produces high levels of reactive oxygen species (ROS). These ROS seem to have a primary role in the regulation of the transcription factor hypoxia inducible factor 1α that triggers death effectors. Here we discuss the role of mitochondria in AD putting focus on the activation of hypoxia-mediated mitochondrial pathways, which could eventually lead to cell degeneration and death.

Original languageEnglish
Article number433
JournalJournal of bioenergetics and biomembranes
Volume41
Early online date15 Oct 2009
DOIs
Publication statusPublished - Oct 2009

Keywords

  • mitochondria
  • hypoxia
  • ROS

Fingerprint Dive into the research topics of 'Role of mitochondrial-mediated signaling pathways in Alzheimer disease and hypoxia'. Together they form a unique fingerprint.

  • Cite this

    Carvalho, C., Correia, S. C., Santos, R. X., Cardoso, S., Moreira, P. I., Clark, T. A., Zhu, X., Smith, M. A., & Perry, G. (2009). Role of mitochondrial-mediated signaling pathways in Alzheimer disease and hypoxia. Journal of bioenergetics and biomembranes, 41, [433]. https://doi.org/10.1007/s10863-009-9247-1