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Hallmarks of Parkinson’s Disease
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Hallmarks of Parkinson’s Disease

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

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 23819

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Cristine Alves Da Costa

E-Mail Website
Guest Editor
Institut de Pharmacologie Moléculaire et Cellulaire, Université Côte d'Azur, INSERM, CNRS, IPMC, Valbonne, France
Interests: Parkinson’s disease; Alzheimer’s disease, brain tumors; transcription; autophagy; cell death; ER-stress/unfolded protein response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) is a movement disorder characterized by the degeneration of dopaminergic neurons. PD is the second cause of motor disability in aged populations, and it affects one person out of 1000. Thus, given the health and economic impacts associated with the increase of PD prevalence in aging populations, the decryptage of the molecular cascades responsible for the etiology of the disease and/or contributing to its progression is crucial. During the last few decades the huge effort of the scientifc community to gain insight into the pathophysiology of PD has culminated in the idenfication of multiple interconnected disfonctional processes. These frequent dysfunctions have been recently named “PD hallmarks” by Antonny and colleagues. This categorization, probably inspired by the seminal work of Hanahan and Weinberg concerning cancer hallmarks, also pinpoints the fact that degenerating neurons share several cellular defective processes.

This Special Issue offers an open access forum that gathers a collection of review articles aiming to update the current knowledge on PD pathogenesis. Suggested potential topics include, but are not restricted to, PD hallmarks, e.g., mitochondrial dysfunction, lysosomal and proteasome failure, neuroinflamation, protein misfolding, apoptosis, calcium inbalance, synaptic dysfunction, oxidative stress, mitophagy, propagation, and spreading.

Dr. Cristine Alves Da Costa
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Parkinson’s disease
  • pathogenesis
  • neurogeneration
  • cellular common dysfunctional processes
  • genetics
  • animal models

Published Papers (5 papers)

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Review

19 pages, 4626 KiB  
Review
Hallmarks and Molecular Tools for the Study of Mitophagy in Parkinson’s Disease
by Thomas Goiran, Mohamed A. Eldeeb, Cornelia E. Zorca and Edward A. Fon
Cells 2022, 11(13), 2097; https://doi.org/10.3390/cells11132097 - 02 Jul 2022
Cited by 14 | Viewed by 4234
Abstract
The best-known hallmarks of Parkinson’s disease (PD) are the motor deficits that result from the degeneration of dopaminergic neurons in the substantia nigra. Dopaminergic neurons are thought to be particularly susceptible to mitochondrial dysfunction. As such, for their survival, they rely on the [...] Read more.
The best-known hallmarks of Parkinson’s disease (PD) are the motor deficits that result from the degeneration of dopaminergic neurons in the substantia nigra. Dopaminergic neurons are thought to be particularly susceptible to mitochondrial dysfunction. As such, for their survival, they rely on the elaborate quality control mechanisms that have evolved in mammalian cells to monitor mitochondrial function and eliminate dysfunctional mitochondria. Mitophagy is a specialized type of autophagy that mediates the selective removal of damaged mitochondria from cells, with the net effect of dampening the toxicity arising from these dysfunctional organelles. Despite an increasing understanding of the molecular mechanisms that regulate the removal of damaged mitochondria, the detailed molecular link to PD pathophysiology is still not entirely clear. Herein, we review the fundamental molecular pathways involved in PINK1/Parkin-mediated and receptor-mediated mitophagy, the evidence for the dysfunction of these pathways in PD, and recently-developed state-of-the art assays for measuring mitophagy in vitro and in vivo. Full article
(This article belongs to the Special Issue Hallmarks of Parkinson’s Disease)
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37 pages, 4205 KiB  
Review
Alpha-Synuclein and Lipids: The Elephant in the Room?
by Alessia Sarchione, Antoine Marchand, Jean-Marc Taymans and Marie-Christine Chartier-Harlin
Cells 2021, 10(9), 2452; https://doi.org/10.3390/cells10092452 - 17 Sep 2021
Cited by 17 | Viewed by 4444
Abstract
Since the initial identification of alpha-synuclein (α-syn) at the synapse, numerous studies demonstrated that α-syn is a key player in the etiology of Parkinson’s disease (PD) and other synucleinopathies. Recent advances underline interactions between α-syn and lipids that also participate in α-syn misfolding [...] Read more.
Since the initial identification of alpha-synuclein (α-syn) at the synapse, numerous studies demonstrated that α-syn is a key player in the etiology of Parkinson’s disease (PD) and other synucleinopathies. Recent advances underline interactions between α-syn and lipids that also participate in α-syn misfolding and aggregation. In addition, increasing evidence demonstrates that α-syn plays a major role in different steps of synaptic exocytosis. Thus, we reviewed literature showing (1) the interplay among α-syn, lipids, and lipid membranes; (2) advances of α-syn synaptic functions in exocytosis. These data underscore a fundamental role of α-syn/lipid interplay that also contributes to synaptic defects in PD. The importance of lipids in PD is further highlighted by data showing the impact of α-syn on lipid metabolism, modulation of α-syn levels by lipids, as well as the identification of genetic determinants involved in lipid homeostasis associated with α-syn pathologies. While questions still remain, these recent developments open the way to new therapeutic strategies for PD and related disorders including some based on modulating synaptic functions. Full article
(This article belongs to the Special Issue Hallmarks of Parkinson’s Disease)
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Graphical abstract

12 pages, 618 KiB  
Review
The PINK1-Mediated Crosstalk between Neural Cells and the Underlying Link to Parkinson’s Disease
by Elvira Pequeno Leites and Vanessa Alexandra Morais
Cells 2021, 10(6), 1395; https://doi.org/10.3390/cells10061395 - 05 Jun 2021
Cited by 7 | Viewed by 2941
Abstract
Mitochondrial dysfunction has a fundamental role in the development of idiopathic and familiar forms of Parkinson’s disease (PD). The nuclear-encoded mitochondrial kinase PINK1, linked to familial PD, is responsible for diverse mechanisms of mitochondrial quality control, ATP production, mitochondrial-mediated apoptosis and neuroinflammation. The [...] Read more.
Mitochondrial dysfunction has a fundamental role in the development of idiopathic and familiar forms of Parkinson’s disease (PD). The nuclear-encoded mitochondrial kinase PINK1, linked to familial PD, is responsible for diverse mechanisms of mitochondrial quality control, ATP production, mitochondrial-mediated apoptosis and neuroinflammation. The main pathological hallmark of PD is the loss of dopaminergic neurons. However, novel discoveries have brought forward the concept that a disruption in overall brain homeostasis may be the underlying cause of this neurodegeneration disease. To sustain this, astrocytes and microglia cells lacking PINK1 have revealed increased neuroinflammation and deficits in physiological roles, such as decreased wound healing capacity and ATP production, which clearly indicate involvement of these cells in the physiopathology of PD. PINK1 executes vital functions within mitochondrial regulation that have a detrimental impact on the development and progression of PD. Hence, in this review, we aim to broaden the horizon of PINK1-mediated phenotypes occurring in neurons, astrocytes and microglia and, ultimately, highlight the importance of the crosstalk between these neural cells that is crucial for brain homeostasis. Full article
(This article belongs to the Special Issue Hallmarks of Parkinson’s Disease)
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Figure 1

19 pages, 882 KiB  
Review
Alpha-Synuclein: Mechanisms of Release and Pathology Progression in Synucleinopathies
by Inês C. Brás and Tiago F. Outeiro
Cells 2021, 10(2), 375; https://doi.org/10.3390/cells10020375 - 12 Feb 2021
Cited by 53 | Viewed by 5707
Abstract
The accumulation of misfolded alpha-synuclein (aSyn) throughout the brain, as Lewy pathology, is a phenomenon central to Parkinson’s disease (PD) pathogenesis. The stereotypical distribution and evolution of the pathology during disease is often attributed to the cell-to-cell transmission of aSyn between interconnected brain [...] Read more.
The accumulation of misfolded alpha-synuclein (aSyn) throughout the brain, as Lewy pathology, is a phenomenon central to Parkinson’s disease (PD) pathogenesis. The stereotypical distribution and evolution of the pathology during disease is often attributed to the cell-to-cell transmission of aSyn between interconnected brain regions. The spreading of conformationally distinct aSyn protein assemblies, commonly referred as strains, is thought to result in a variety of clinically and pathologically heterogenous diseases known as synucleinopathies. Although tremendous progress has been made in the field, the mechanisms involved in the transfer of these assemblies between interconnected neural networks and their role in driving PD progression are still unclear. Here, we present an update of the relevant discoveries supporting or challenging the prion-like spreading hypothesis. We also discuss the importance of aSyn strains in pathology progression and the various putative molecular mechanisms involved in cell-to-cell protein release. Understanding the pathways underlying aSyn propagation will contribute to determining the etiology of PD and related synucleinopathies but also assist in the development of new therapeutic strategies. Full article
(This article belongs to the Special Issue Hallmarks of Parkinson’s Disease)
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24 pages, 1629 KiB  
Review
The Endoplasmic Reticulum Stress/Unfolded Protein Response and Their Contributions to Parkinson’s Disease Physiopathology
by Cristine Alves da Costa, Wejdane El Manaa, Eric Duplan and Frédéric Checler
Cells 2020, 9(11), 2495; https://doi.org/10.3390/cells9112495 - 17 Nov 2020
Cited by 52 | Viewed by 5059
Abstract
Parkinson’s disease (PD) is a multifactorial age-related movement disorder in which defects of both mitochondria and the endoplasmic reticulum (ER) have been reported. The unfolded protein response (UPR) has emerged as a key cellular dysfunction associated with the etiology of the disease. The [...] Read more.
Parkinson’s disease (PD) is a multifactorial age-related movement disorder in which defects of both mitochondria and the endoplasmic reticulum (ER) have been reported. The unfolded protein response (UPR) has emerged as a key cellular dysfunction associated with the etiology of the disease. The UPR involves a coordinated response initiated in the endoplasmic reticulum that grants the correct folding of proteins. This review gives insights on the ER and its functioning; the UPR signaling cascades; and the link between ER stress, UPR activation, and physiopathology of PD. Thus, post-mortem studies and data obtained by either in vitro and in vivo pharmacological approaches or by genetic modulation of PD causative genes are described. Further, we discuss the relevance and impact of the UPR to sporadic and genetic PD pathology. Full article
(This article belongs to the Special Issue Hallmarks of Parkinson’s Disease)
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