Parkinson's Disease: The Link Between Monoamine Oxidase and Mitochondrial Respiration

2004 ◽  
Author(s):  
Martin R. Gluck
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Monoamine Oxidase ◽  
Mitochondrial Respiration

scholarly journals The Parkinson’s Disease-Associated Protein DJ-1 Protects Dictyostelium Cells from AMPK-Dependent Outcomes of Oxidative Stress

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1874
Author(s):  
Suwei Chen ◽  
Sarah J. Annesley ◽  
Rasha A. F. Jasim ◽  
Paul R. Fisher
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Respiration ◽  
Cysteine Residue ◽  
Reduced Form ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Pathology

Mitochondrial dysfunction has been implicated in the pathology of Parkinson’s disease (PD). In Dictyostelium discoideum, strains with mitochondrial dysfunction present consistent, AMPK-dependent phenotypes. This provides an opportunity to investigate if the loss of function of specific PD-associated genes produces cellular pathology by causing mitochondrial dysfunction with AMPK-mediated consequences. DJ-1 is a PD-associated, cytosolic protein with a conserved oxidizable cysteine residue that is important for the protein’s ability to protect cells from the pathological consequences of oxidative stress. Dictyostelium DJ-1 (encoded by the gene deeJ) is located in the cytosol from where it indirectly inhibits mitochondrial respiration and also exerts a positive, nonmitochondrial role in endocytosis (particularly phagocytosis). Its loss in unstressed cells impairs endocytosis and causes correspondingly slower growth, while also stimulating mitochondrial respiration. We report here that oxidative stress in Dictyostelium cells inhibits mitochondrial respiration and impairs phagocytosis in an AMPK-dependent manner. This adds to the separate impairment of phagocytosis caused by DJ-1 knockdown. Oxidative stress also combines with DJ-1 loss in an AMPK-dependent manner to impair or exacerbate defects in phototaxis, morphogenesis and growth. It thereby phenocopies mitochondrial dysfunction. These results support a model in which the oxidized but not the reduced form of DJ-1 inhibits AMPK in the cytosol, thereby protecting cells from the adverse consequences of oxidative stress, mitochondrial dysfunction and the resulting AMPK hyperactivity.

Altered Platelet Monoamine Oxidase-B Activity in Idiopathic Parkinson’s Disease

2009 ◽  
Vol 34 (8) ◽  
pp. 1427-1432 ◽  
Author(s):  
Maroof Husain ◽  
Rakesh Shukla ◽  
Madhu Dikshit ◽  
Pradeep K. Maheshwari ◽  
Devika Nag ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase B ◽  
Idiopathic Parkinson’S Disease ◽  
Idiopathic Parkinson's Disease ◽  
Platelet Monoamine Oxidase

scholarly journals Monoamine oxidase B inhibitors for early Parkinson's disease

2005 ◽  
Author(s):  
Kristian Turnbull ◽  
Robert Caslake ◽  
Angus Macleod ◽  
Natalie Ives ◽  
Rebecca Stowe ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase B ◽  
Early Parkinson’S Disease

▼ Safinamide for Parkinson’s disease

2018 ◽  
Vol 56 (5) ◽  
pp. 54-57
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Monoamine Oxidase ◽  
Motor Fluctuations ◽  
Daily Activities ◽  
Monoamine Oxidase B ◽  
Motor Symptoms ◽  
Idiopathic Parkinson’S Disease ◽  
Mao B ◽  
Idiopathic Parkinson's Disease

▼ Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson’s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson’s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.

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