New Insights into Parkinson’s Disease: From Molecular Basis to Therapy—2nd Edition

A Special Issue of Life (ISSN 2075-1729) belonging to the section "Medical Research".

Deadline for manuscript submissions: 31 March 2027 | Viewed by 3762

Editor


E-Mail
Guest Editor
1. Department of Biomedical Sciences, School of Health Sciences, International Hellenic University, 5400 Thessaloniki, Greece
2. Laboratory of Medical Biology-Genetics, Medical School, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece
Interests: genetics; neurodegeneration; Parkinson’s disease; Alzheimer’s disease; biomarkers; pharmacogenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are grateful to the researchers who contributed to the first volume of this Special Issue:
https://www.mdpi.com/journal/life/special_issues/58XJ195N0W.

Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 1–2% of the population over the age of 65 years. About 90-95% of PD patients exhibit sporadic disease, attributed to interactions between environmental and genetic factors, whereas approximately 5-10% of PD cases are familial, following an autosomal dominant or autosomal recessive mode of inheritance. Advances in the field of genetics have aided in the identification of specific genes and the recognition of molecular pathways relevant to PD pathogenesis.

This Special Issue, entitled “New Insights into Parkinson’s Disease: From Molecular Basis to Therapy—2nd Edition”, will showcase submissions (research articles, reviews, meta-analyses, etc.) that enhance our knowledge on the genetic background of PD, aiming to better delineate the genetic and epigenetic contribution to disease progression, increase our understanding of the exact pathophysiologic mechanisms implicated in PD, utilize genetic information to facilitate the diagnosis and prediction of the disease, and enable more tailored and effective therapeutic approaches to this neurodegenerative disease.

Dr. Kallirhoe Kalinderi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly 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 2600 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.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Review

21 pages, 1074 KB  
Review
Dysregulation of the Extracellular Matrix in the Synaptic Pathology of Parkinson’s Disease: Molecular Mechanisms and Novel Therapeutic Approaches
by Carmen Rubio, Ricardo Pérez-Rubio, Javier Pérez-Villavicencio, Norma Serrano-García, Ángel Lee, Leticia Granados-Rojas, Martha Tena-Suck and Moisés Rubio-Osornio
Life 2026, 16(6), 1007; https://doi.org/10.3390/life16061007 - 15 Jun 2026
Viewed by 860
Abstract
Parkinson’s disease (PD) is defined by the progressive degeneration of dopaminergic neurons within the substantia nigra and the pathological accumulation of α-synuclein (α-syn) aggregates. Beyond these intracellular hallmarks, the extracellular matrix (ECM) has emerged as an active regulator of synaptic dysfunction, neuroinflammation, and [...] Read more.
Parkinson’s disease (PD) is defined by the progressive degeneration of dopaminergic neurons within the substantia nigra and the pathological accumulation of α-synuclein (α-syn) aggregates. Beyond these intracellular hallmarks, the extracellular matrix (ECM) has emerged as an active regulator of synaptic dysfunction, neuroinflammation, and disease progression. Recent multi-omics evidence, including transcriptomic and proteomic profiling of post-mortem tissue and iPSC-derived neurons, demonstrates consistent dysregulation of ECM components across both sporadic and genetic PD subtypes—typified by downregulation of basement membrane collagens (COL4A) and integrin signaling (ITGB1), alongside upregulation of matrix metalloproteinases (MMPs). These alterations destabilize perineuronal nets (PNNs), allow prion-like α-syn propagation, and promote glial activation through TLR-mediated signaling. Circulating ECM-derived neoepitopes (C1M, C4M) may complement neurofilament light chain as prognostic biomarkers of disease progression, although prospective validation remains necessary. Pharmacological strategies targeting MMP activity (e.g., doxycycline), integrin–FAK signaling (ATN-161), and MMP–TIMP balance (mesenchymal stem cells) represent emerging therapeutic avenues, though clinical evidence in PD remains limited. This review synthesizes current evidence on ECM dysregulation in PD and discusses its implications for biomarker development and disease-modifying intervention. Full article
Show Figures

Figure 1

18 pages, 697 KB  
Review
Pathways and Genetic Determinants of Impulse Control Disorders in Parkinson’s Disease
by Kallirhoe Kalinderi, Vasileios Papaliagkas, Oraiozili Goula, Liana Fidani and Maria Chatzidimitriou
Life 2026, 16(6), 897; https://doi.org/10.3390/life16060897 - 27 May 2026
Viewed by 1576
Abstract
Background: Impulse control disorders (ICDs) are a common non-motor complication in Parkinson’s disease (PD) patients with multiple negative consequences for the individual and caregivers. Although ICDs are strongly linked to dopaminergic therapy, particularly dopamine agonists, only a percentage of patients develop these [...] Read more.
Background: Impulse control disorders (ICDs) are a common non-motor complication in Parkinson’s disease (PD) patients with multiple negative consequences for the individual and caregivers. Although ICDs are strongly linked to dopaminergic therapy, particularly dopamine agonists, only a percentage of patients develop these behaviors, suggesting the involvement of additional susceptibility factors, including genetic variability. This review aims to analyze current knowledge on the genetic background of ICDs. Methods: A literature search was conducted in the PubMed and Scopus databases for peer-reviewed research regarding the role of genetics in ICDs, published in the English language from 1996 to 2026. References of the selected articles for possible additional articles were also screened in order to include most of the key recent evidence. Genes that are involved in the dopaminergic system play a central role in ICD susceptibility, although the findings in studies are often inconsistent and not replicated. Moreover, variants in genes related to the glutamatergic (e.g., GRIN2B), serotonergic (e.g., HTR2A and TPH2), and opioid systems (e.g., OPRK1 and OPRM1) have been implicated, supporting a multi-system contribution to ICD pathophysiology. Conclusions: Early recognition of genetic factors that increase susceptibility to ICDs in PD patients is awaited to increase diagnostic accuracy and expedite individualized treatment. Full article
Show Figures

Graphical abstract

Back to TopTop