THE ROLE OF MITOCHONDRIAL DYSFUNCTION IN THE DEVELOPMENT OF PARKINSON`S DISEASE
R.V. Rozova1, D.S. Krasnenkov2, I.M. Karaban2
- O.O. Bogomolets Institute of Physiology, NAS of Ukraine, Kyiv, Ukraine
- D.F. Chebotaryov Institute of Gerontology, NAMS of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz72.04.081

Abstract
A significant part of neurodegenerative disorders may be attributed to so-called mitochondrial diseases. Parkinson’s disease
(PD), one of the most common neurodegenerative pathologies
after Alzheimer’s disease, is among those disorders that may be
linked to mitochondrial dysfunction. The relationship between
PD and mitochondrial disorders was first established in 1989.
In the substantia nigra, and subsequently in peripheral tissues
of patients with PD, a 25-35% inhibition of the activity of
respiratory chain complex I was detected. The identification
of an association between reduced complex I activity and the
symptoms of PD left open the question of the role of complex
I functional insufficiency in the pathogenesis of Parkinsonism.
It should be emphasized that the mechanisms underlying PD
remain largely unclear to this day. However, several hypotheses
regarding its pathogenesis have been proposed. The resolution
of these issues remains highly relevant in both physiology and
theoretical and clinical medicine.
Keywords:
neurodegenerative disorders; mitochondrial dysfunction; Parkinson's disease; oxidative stress; mitochondrial DNA; gene PINK1; gene PARKIN; gene DG-1; medulla oblongata; striatum; heart; lungs
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