Human brain cortex: mitochondrial oxidative damage and adaptive response in Parkinson disease and in dementia with Lewy bodies

Frontal cortex samples from frozen human brains were used to assess tissue respiration; content of mitochondria; mitochondrial oxygen uptake; activity of respiratory complexes and of mitochondrial nitric oxide synthase; content of cytochromes a, b, and c; oxidative damage; and expression of Mn-SOD in patients with Parkinson disease and with dementia with Lewy bodies in comparison with those of normal healthy controls

Ana Navarro

2009

Scholarcy highlights

  • Frontal cortex samples from frozen human brains were used to assess tissue respiration; content of mitochondria; mitochondrial oxygen uptake; activity of respiratory complexes and of mitochondrial nitric oxide synthase; content of cytochromes a, b, and c; oxidative damage; and expression of Mn-SOD in patients with Parkinson disease and with dementia with Lewy bodies in comparison with those of normal healthy controls
  • Brain cortex and mitochondrial O2 uptake and complex I activity were significantly lower in PD and DLB, whereas mitochondrial nitric oxide synthase activity, cytochrome content, expression of Mn-SOD, mitochondrial mass, and oxidative damage were significantly higher in the frontal cortex in PD and DLB
  • The decreases in tissue and mitochondrial O2 uptake and in complex I activity are considered the consequences of mitochondrial oxidative damage
  • The increases in mtNOS activity and in mitochondrial mass are interpreted as an adaptive response of the frontal cortex that involves increased NO signaling for mitochondrial biogenesis
  • The adaptive response would partially compensate for mitochondrial dysfunction in these neurodegenerative diseases and would afford a human evolutionary response to shortage of ATP in the frontal cortex

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