Special Issue "Molecular and Cellular Mechanisms of Parkinson's Disease"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 January 2021.

Special Issue Editor

Prof. Wolfgang Jost
Website SciProfiles
Guest Editor
Center for Movement Disorders, Parkinson-Klinik Ortenau, 77709 Wolfach, Germany
Interests: Parkinson’s disease; atypical Parkinson syndromes; dystonia; autonomic nervous system; botulinum toxin
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Special Issue Information

Dear Colleagues,

Parkinson’s disease is a disease for which we have attained a massive gain in knowledge within the last few decades, and for which the number of publications has increased as in hardly any other area of medicine. We are fortunate to have many effective medications at our disposal for this disease. The central issue here has been the substantia nigra, and the deficiency in levodopa has been the pivotal focus for therapy. In the last two decades, however, we have learned that emphasis on these concepts offers only limited benefits and may in fact be detrimental for further progress in research. To be precise, the substantia nigra is neither the origin nor the end point of the degenerative process, and furthermore dopaminergic therapy is merely a symptomatic intervention. Of course, all further progress is a factor of our basic hypotheses, but these have to be substantiated as to their validity. In Parkinson’s diagnostics and therapy, we have arrived at something of a stalemate: many new findings are truly spectacular, but not yet the final answer to all our questions. As clinicians, of course, we tend to target quick solutions, but so do our patients, and these quick solutions are still very illusive. For this reason, we have to return to the situation at the historical start of work on Parkinson’s and take a good look at current gaps in knowledge in order to work them out scientifically. For this reason, we have decided to put out a Special Issue entitled “Molecular and Cellular Mechanisms of Parkinson’s Disease”. We are deliberately not working on a new and comprehensive model in this Issue, but intend to outline the current status of different aspects so that the large spectrum of findings can be seen and so that some hints can be gleaned as to just where we might profitably pursue new fields of research and where we should avoid some potential dead-ends. Put metaphorically, if I have become lost in a city it is more helpful to return to the starting point and not just to rely on keeping to the obviously wrong route taken. So, we want to meet at the market and trade our current awareness.

Prof. Wolfgang Jost
Guest Editor

Manuscript Submission Information

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Keywords

  • Parkinson’s disease
  • Alpha-synuclein
  • Genetics
  • Inflammation

Published Papers (2 papers)

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Editorial

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Open AccessEditorial
Is It Meanwhile Biomedical Sciences or Still “Ars Medica”?
Cells 2020, 9(10), 2313; https://doi.org/10.3390/cells9102313 - 17 Oct 2020
Abstract
Scientific work is usually quite time-intensive and frequently replete with frustrations [...] Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Parkinson's Disease)
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Research

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Open AccessArticle
The Multimodal Serotonergic Agent Vilazodone Inhibits L-DOPA-Induced Gene Regulation in Striatal Projection Neurons and Associated Dyskinesia in an Animal Model of Parkinson’s Disease
Cells 2020, 9(10), 2265; https://doi.org/10.3390/cells9102265 - 09 Oct 2020
Abstract
Levodopa (L-DOPA) treatment in Parkinson’s disease is limited by the emergence of L-DOPA-induced dyskinesia. Such dyskinesia is associated with aberrant gene regulation in neurons of the striatum, which is caused by abnormal dopamine release from serotonin terminals. Previous work showed that modulating the [...] Read more.
Levodopa (L-DOPA) treatment in Parkinson’s disease is limited by the emergence of L-DOPA-induced dyskinesia. Such dyskinesia is associated with aberrant gene regulation in neurons of the striatum, which is caused by abnormal dopamine release from serotonin terminals. Previous work showed that modulating the striatal serotonin innervation with selective serotonin reuptake inhibitors (SSRIs) or 5-HT1A receptor agonists could attenuate L-DOPA-induced dyskinesia. We investigated the effects of a novel serotonergic agent, vilazodone, which combines SSRI and 5-HT1A partial agonist properties, on L-DOPA-induced behavior and gene regulation in the striatum in an animal model of Parkinson’s disease. After unilateral dopamine depletion by 6-hydroxydopamine (6-OHDA), rats received repeated L-DOPA treatment (5 mg/kg) alone or in combination with vilazodone (10 mg/kg) for 3 weeks. Gene regulation was then mapped throughout the striatum using in situ hybridization histochemistry. Vilazodone suppressed the development of L-DOPA-induced dyskinesia and turning behavior but did not interfere with the prokinetic effects of L-DOPA (forelimb stepping). L-DOPA treatment drastically increased the expression of dynorphin (direct pathway), 5-HT1B, and zif268 mRNA in the striatum ipsilateral to the lesion. These effects were inhibited by vilazodone. In contrast, vilazodone had no effect on enkephalin expression (indirect pathway) or on gene expression in the intact striatum. Thus, vilazodone inhibited L-DOPA-induced gene regulation selectively in the direct pathway of the dopamine-depleted striatum, molecular changes that are considered critical for L-DOPA-induced dyskinesia. These findings position vilazodone, an approved antidepressant, as a potential adjunct medication for the treatment of L-DOPA-induced motor side effects. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Parkinson's Disease)
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