Cortical cytochrome oxidase activity is reduced in Alzheimer's disease

J Neurochem. 1994 Dec;63(6):2179-84. doi: 10.1046/j.1471-4159.1994.63062179.x.


A defect in energy metabolism may play a role in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease. In the present study, we examined the activities of the enzymes that catalyze oxidative phosphorylation in frontal, temporal, parietal, and occipital cortex from Alzheimer's disease patients and age-matched controls. Complex I and complex II-III activities showed a small decrease in occipital cortex, but were unaffected in the other cortical areas. The most consistent change was a significant decrease of cytochrome oxidase (complex IV) activity of 25-30% in the four cortical regions examined. These results provide further evidence of a cytochrome oxidase defect in Alzheimer's disease postmortem brain tissue. A deficiency in this key energy-metabolizing enzyme could lead to a reduction in energy stores and thereby contribute to the neurodegenerative process.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alzheimer Disease / enzymology*
  • Cerebral Cortex / enzymology*
  • Cerebral Cortex / ultrastructure
  • Electron Transport Complex II
  • Electron Transport Complex III / metabolism
  • Electron Transport Complex IV / metabolism*
  • Energy Metabolism
  • Frontal Lobe / enzymology
  • Humans
  • Mitochondria / enzymology
  • Multienzyme Complexes / metabolism
  • NAD(P)H Dehydrogenase (Quinone) / metabolism
  • Occipital Lobe / enzymology
  • Oxidoreductases / metabolism
  • Parietal Lobe / enzymology
  • Succinate Dehydrogenase / metabolism
  • Temporal Lobe / enzymology


  • Multienzyme Complexes
  • Oxidoreductases
  • Electron Transport Complex II
  • Succinate Dehydrogenase
  • NAD(P)H Dehydrogenase (Quinone)
  • Electron Transport Complex IV
  • Electron Transport Complex III