@article{PlumEggersHellingetal.2020,
  author    = {Plum, Sarah and Eggers, Britta and Helling, Stefan and Stepath, Markus and Theiss, Carsten and Leite, Renata E. P. and Molina, Mariana and Grinberg, Lea T. and Riederer, Peter and Gerlach, Manfred and May, Caroline and Marcus, Katrin},
  title     = {Proteomic characterization of synaptosomes from human substantia nigra indicates altered mitochondrial translation in Parkinson's disease},
  series = {Cells},
  volume    = {9},
  journal   = {Cells},
  number    = {12},
  issn      = {2073-4409},
  doi       = {10.3390/cells9122580},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-219978},
  year      = {2020},
  abstract  = {The pathological hallmark of Parkinson's disease (PD) is the loss of neuromelanin-containing dopaminergic neurons within the substantia nigra pars compacta (SNpc). Additionally, numerous studies indicate an altered synaptic function during disease progression. To gain new insights into the molecular processes underlying the alteration of synaptic function in PD, a proteomic study was performed. Therefore, synaptosomes were isolated by density gradient centrifugation from SNpc tissue of individuals at advanced PD stages (N = 5) as well as control subjects free of pathology (N = 5) followed by mass spectrometry-based analysis. In total, 362 proteins were identified and assigned to the synaptosomal core proteome. This core proteome comprised all proteins expressed within the synapses without regard to data analysis software, gender, age, or disease. The differential analysis between control subjects and PD cases revealed that CD9 antigen was overrepresented and fourteen proteins, among them Thymidine kinase 2 (TK2), mitochondrial, 39S ribosomal protein L37, neurolysin, and Methionine-tRNA ligase (MARS2) were underrepresented in PD suggesting an alteration in mitochondrial translation within synaptosomes.},
  language  = {en}
}
@article{SianHulsmannRiederer2021,
  author    = {Sian-Hulsmann, Jeswinder and Riederer, Peter},
  title     = {The nigral coup in Parkinson's Disease by α-synuclein and its associated rebels},
  series = {Cells},
  volume    = {10},
  journal   = {Cells},
  number    = {3},
  issn      = {2073-4409},
  doi       = {10.3390/cells10030598},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-234073},
  year      = {2021},
  abstract  = {The risk of Parkinson's disease increases with age. However, the etiology of the illness remains obscure. It appears highly likely that the neurodegenerative processes involve an array of elements that influence each other. In addition, genetic, endogenous, or exogenous toxins need to be considered as viable partners to the cellular degeneration. There is compelling evidence that indicate the key involvement of modified α-synuclein (Lewy bodies) at the very core of the pathogenesis of the disease. The accumulation of misfolded α-synuclein may be a consequence of some genetic defect or/and a failure of the protein clearance system. Importantly, α-synuclein pathology appears to be a common denominator for many cellular deleterious events such as oxidative stress, mitochondrial dysfunction, dopamine synaptic dysregulation, iron dyshomeostasis, and neuroinflammation. These factors probably employ a common apoptotic/or autophagic route in the final stages to execute cell death. The misfolded α-synuclein inclusions skillfully trigger or navigate these processes and thus amplify the dopamine neuron fatalities. Although the process of neuroinflammation may represent a secondary event, nevertheless, it executes a fundamental role in neurodegeneration. Some viral infections produce parkinsonism and exhibit similar characteristic neuropathological changes such as a modest brain dopamine deficit and α-synuclein pathology. Thus, viral infections may heighten the risk of developing PD. Alternatively, α-synuclein pathology may induce a dysfunctional immune system. Thus, sporadic Parkinson's disease is caused by multifactorial trigger factors and metabolic disturbances, which need to be considered for the development of potential drugs in the disorder.},
  language  = {en}
}