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Mitochondrial complex I deficiency in Parkinson's disease.

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This article is published in The Lancet.The article was published on 1989-06-03. It has received 1548 citations till now. The article focuses on the topics: NAD(P)H Dehydrogenase (Quinone) & Substantia nigra.

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New insights on Parkinson’s disease genes: the link between mitochondria impairment and neuroinflammation

TL;DR: The link between PD-related genes, which are involved in mitochondrial function, and deleterious neuroinflammation is described, which was demonstrated mostly in neuronal cells.
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Construction of photoenergetic mitochondria in cultured mammalian cells

TL;DR: The results suggest that the light-activated proton pump functioned as a PMF generator in the mitochondria of mammalian cells, and suppressed cell death induced by inhibition of respiratory PMF generation.
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N-Terminal Truncated UCH-L1 Prevents Parkinson's Disease Associated Damage

TL;DR: Stable expression of NT-UCH-L1 decreases cellular ROS levels and protects cells from H2O2, rotenone and CCCP-induced cell death and transgenic mice are less susceptible to degeneration of nigrostriatal dopaminergic neurons seen in the MPTP mouse model of PD, in comparison to control animals.
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On the Role of Aminochrome in Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Parkinson's Disease

TL;DR: The identity of what triggers the loss of dopaminergic neurons containing neuromelanin in Parkinson’s disease (PD) is still unknown and several mechanisms have been suggested to be involved in the degeneration of nigrostriatal neurons in PD, including mitochondrial dysfunction, endoplasmic reticulum stress, lysosomal and proteasomal protein degradation dysfunction, and neuroinflammation.
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Idebenone Has Distinct Effects on Mitochondrial Respiration in Cortical Astrocytes Compared to Cortical Neurons Due to Differential NQO1 Activity

TL;DR: A fundamental difference in the way Idebenone affects mitochondrial respiration in cortical neurons compared with cortical astrocytes is demonstrated, raising the possibility that lack of neuronal NQO1 activity has contributed to the limited efficacy of idebenone in neurodegenerative disease treatment.
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