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Histological Examination of Mitochondrial Morphology in a Parkinson's Disease Model
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Histological Examination of Mitochondrial Morphology in a Parkinson's Disease Model

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Mitochondrial permeability in neuronal death: possible relevance to the pathogenesis of Parkinson's disease

W G Tatton1, R M Chalmers-Redman, H J Rideout

  • 1Department of Neurology, Mount Sinai School of Medicine, Annenburg 1470, P.O. Box 1137, One Gustave L. Levy Place, New York, NY, 10029-6574, USA.

Parkinsonism & Related Disorders
|July 2, 2008
PubMed

Insights

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) metabolite MPP(+) induces apoptosis by opening the mitochondrial permeability transition pore (PTP). This process is linked to decreased mitochondrial complex I activity, a key factor in Parkinson's disease (PD) pathogenesis.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure leads to neurodegeneration resembling Parkinson's disease (PD).
  • The MPTP metabolite, MPP(+), inhibits mitochondrial complex I, mirroring observations in PD.
  • Mitochondrial permeability transition pore (PTP) opening is a critical event in apoptosis.

Purpose of the Study:

  • To review recent findings on the role of PTP opening in MPP(+)-induced apoptosis.
  • To explore the link between mitochondrial membrane potential (DeltaPsi(M)) reduction and PTP opening.
  • To investigate the contribution of mitochondrial complex I activity to apoptosis in PD.

Main Methods:

  • Review of existing scientific literature.
  • Analysis of studies investigating MPP(+) effects on mitochondrial function.
  • Examination of the relationship between DeltaPsi(M), PTP opening, and apoptosis.

Main Results:

  • MPP(+)-induced apoptosis is mediated by PTP opening.
  • A decrease in DeltaPsi(M) is a key factor in triggering PTP opening.
  • Reduced proton pumping at mitochondrial complex I contributes to DeltaPsi(M) decrease and apoptosis.

Conclusions:

  • MPP(+)-induced apoptosis involves PTP opening secondary to mitochondrial dysfunction.
  • Decreased mitochondrial complex I activity is implicated in both MPP(+)-induced apoptosis and PD pathogenesis.
  • Targeting mitochondrial complex I or PTP may offer therapeutic strategies for PD.

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