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Dopamine Receptors and Neurodegeneration
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Dopamine Receptors and Neurodegeneration

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1379

Special Issue Editor

Dr. Marta Pardo

E-Mail Website
Guest Editor
Department of Psychobiology, Psychology Faculty, Campus of Blasco Ibáñez, University of Valencia, Valencia, Spain
Interests: cognitive neuroscience; dopamine; dopamine transporter; stress; addiction; nanoparticles; neurodegeneration

Special Issue Information

Dear Colleagues,

Dopaminergic dysfunctions can contribute to diverse neuropsychiatric and neurodegenerative disorders, characterized by progressive neuronal loss that leads to degeneration at different levels of the nervous system. Disrupted dopamine (DA) homeostasis, and more specifically dopamine receptor alterations, have been reported in a variety of psychiatric and neurodegenerative disorders.

The present Special Issue provides an excellent opportunity to converge the most updated state of current research studies related to the implication of DA receptors in a variety of neurodegenerative disorders due to the unclear pathogenesis underlying neurodegeneration.

We call for genetic studies as well as basic behavioral and pharmaceutical approaches to help understand better the critical role of each DA receptor in psychopathology to allow the discovery of new treatment approaches for such devastating impacts of neurodegenerative diseases worldwide.

Potential topics include, but are not limited to, the following:

  • Dopamine receptor mechanisms of action on neurodegeneration;
  • The behavioral impacts of DA receptor alterations;
  • Adverse effects of the DA system on neurodegenerative diseases;
  • Molecular basis of DA impairments and their impact on neurodegeneration;
  • Future perspectives for neurodegeneration interventions: dopamine implications;
  • Genetical approaches: implications of DA in neurodegeneration.

Dr. Marta Pardo
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Molecules 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

  • dopamine
  • dopamine receptor
  • neurodegeneration
  • Alzheimer
  • Huntington
  • Parkinson

Published Papers (1 paper)

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Research

25 pages, 4693 KiB  
Article
Long-Term Impact of Diffuse Traumatic Brain Injury on Neuroinflammation and Catecholaminergic Signaling: Potential Relevance for Parkinson’s Disease Risk
by Ing Chee Wee, Alina Arulsamy, Frances Corrigan and Lyndsey Collins-Praino
Molecules 2024, 29(7), 1470; https://doi.org/10.3390/molecules29071470 - 26 Mar 2024
Viewed by 637
Abstract
Traumatic brain injury (TBI) is associated with an increased risk of developing Parkinson’s disease (PD), though the exact mechanisms remain unclear. TBI triggers acute neuroinflammation and catecholamine dysfunction post-injury, both implicated in PD pathophysiology. The long-term impact on these pathways following TBI, however, [...] Read more.
Traumatic brain injury (TBI) is associated with an increased risk of developing Parkinson’s disease (PD), though the exact mechanisms remain unclear. TBI triggers acute neuroinflammation and catecholamine dysfunction post-injury, both implicated in PD pathophysiology. The long-term impact on these pathways following TBI, however, remains uncertain. In this study, male Sprague-Dawley rats underwent sham surgery or Marmarou’s impact acceleration model to induce varying TBI severities: single mild TBI (mTBI), repetitive mild TBI (rmTBI), or moderate–severe TBI (msTBI). At 12 months post-injury, astrocyte reactivity (GFAP) and microglial levels (IBA1) were assessed in the striatum (STR), substantia nigra (SN), and prefrontal cortex (PFC) using immunohistochemistry. Key enzymes and receptors involved in catecholaminergic transmission were measured via Western blot within the same regions. Minimal changes in these markers were observed, regardless of initial injury severity. Following mTBI, elevated protein levels of dopamine D1 receptors (DRD1) were noted in the PFC, while msTBI resulted in increased alpha-2A adrenoceptors (ADRA2A) in the STR and decreased dopamine beta-hydroxylase (DβH) in the SN. Neuroinflammatory changes were subtle, with a reduced number of GFAP+ cells in the SN following msTBI. However, considering the potential for neurodegenerative outcomes to manifest decades after injury, longer post-injury intervals may be necessary to observe PD-relevant alterations within these systems. Full article
(This article belongs to the Special Issue Dopamine Receptors and Neurodegeneration)
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