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Cytochrome c oxidase is decreased in Alzheimer's disease platelets

Sandra Morais Cardoso1, M Teresa Proença, Sancha Santos

  • 1Faculty of Medicine, Center for Neuroscience of Coimbra, University of Coimbra, 3004 517, Portugal.

Neurobiology of Aging
|December 17, 2003
PubMed

Insights

Alzheimer's disease (AD) is linked to reduced platelet cytochrome c oxidase (COX) activity. This study confirms the defect, showing lower ATP and higher reactive oxygen species (ROS) in AD platelets, independent of membrane changes.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Gerontology

Background:

  • Reduced cytochrome c oxidase (COX) activity is reported in Alzheimer's disease (AD) brain and platelets.
  • The cause of this COX defect, especially in non-degenerating tissues like platelets, remains unclear.

Purpose of the Study:

  • To confirm the presence of a COX defect in platelets from individuals with Alzheimer's disease.
  • To investigate the underlying factors contributing to the COX defect in AD platelets.

Main Methods:

  • Isolated mitochondria from platelets of AD patients and age-matched controls.
  • Measured COX activity, COX subunit levels, ATP levels, and reactive oxygen species (ROS) production.
  • Assessed platelet membrane fluidity, Vitamin E, and cholesterol content.

Main Results:

  • Confirmed a 15% decrease in COX activity in AD platelet mitochondria compared to controls.
  • Found normal levels of COX subunits in AD platelets.
  • Observed diminished ATP levels and increased ROS production in AD platelets.
  • Determined that membrane fluidity, Vitamin E, and cholesterol were similar between groups.

Conclusions:

  • Platelet mitochondrial COX activity is significantly reduced in Alzheimer's disease.
  • The COX defect is not due to altered membrane properties.
  • The diminished COX activity is associated with reduced ATP production and increased ROS generation in AD platelets.

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