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Specific neuronal populations display high vulnerability to pathological processes in Parkinson's disease (PD). The dorsal motor nucleus of the vagus nerve (DMnX) is a primary site of pathological α-synuclein deposition and may play a key role in the spreading of α-synuclein lesions within and outside the CNS. Using in vivo models, we show that cholinergic neurons forming this nucleus are particularly susceptible to oxidative challenges and accumulation of reactive oxidative species (ROS). Targeted α-synuclein overexpression within these neurons triggered an oxidative stress that became significantly more pronounced after exposure to the ROS-generating agent paraquat. A more severe oxidative stress resulted in enhanced production of oxidatively modified forms of α-synuclein, increased α-synuclein aggregation into oligomeric species and marked degeneration of DMnX neurons. Enhanced oxidative stress also affected neuron-to-neuron protein transfer, causing an increased spreading of α-synuclein from the DMnX toward more rostral brain regions. In vitro experiments confirmed a greater propensity of α-synuclein to pass from cell to cell under pro-oxidant conditions, and identified nitrated α-synuclein forms as highly transferable protein species. These findings substantiate the relevance of oxidative injury in PD pathogenetic processes, establish a relationship between oxidative stress and vulnerability to α-synuclein pathology and define a new mechanism, enhanced cell-to-cell α-synuclein transmission, by which oxidative stress could promote PD development and progression.
This article was published in the following journal.
Name: The Journal of clinical investigation
Parkinson's disease is the second most common neurodegenerative disease caused by degeneration of dopamine neurons in the substantia nigra. The origin and causes of dopamine neurodegeneration in Parki...
Parkinson's disease (PD) is a common neurodegenerative disease that is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The proapoptotic BH3-...
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Parkinson´s disease is based on a Lewy body degeneration of cerebral and extracerebral neurons. This Lewy body degeneration includes cerebral cholinergic neurons besides dopaminergic neur...
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A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
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A protein deglycase that repairs methylglyoxal- and glyoxal-glycated amino acids and proteins, releasing repaired proteins and lactate or glycolate. It deglycates CYSTEINE, ARGININE and LYSINE residues to reactivate proteins by reversing glycation and prevent the formation of ADVANCED GLYCATION END PRODUCTS. It protects cells against OXIDATIVE STRESS and CELL DEATH by functioning as an oxidative stress sensor and redox-sensitive MOLECULAR CHAPERONE and PROTEASE. Mutations in the PARK7 gene are associated with autosomal-recessive, early-onset PARKINSON DISEASE.
A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.
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Neurology - Central Nervous System (CNS)
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