Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 926

Special Issue Editor


E-Mail Website
Guest Editor
Institut de Pharmacologie et de Biologie Structurale, Université Toulouse III—Paul Sabatier, Toulouse, France
Interests: neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are characterized by the progressive degeneration of the nervous system. These diseases result in the progressive and irreversible loss of neurons, leading to cognitive decline or motor dysfunction. The best-known neurodegenerative diseases are Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Neurodegeneration can result from different mechanisms: (a) Protein misfolding and aggregation. Beta-amyloid peptide and tau protein have been implicated in Alzheimer's disease, alpha-synuclein in Parkinson's disease, and huntingtin in Huntington’s disease. (b) Oxidative stress damages cellular structures, including neurons, and may contribute to their degeneration. (c) Chronic inflammation within the nervous system can exacerbate neuronal damage and contribute to the progression of neurodegenerative diseases. (d) Mutations in specific genes can increase an individual’s susceptibility to developing these diseases. For example, mutations in the APP, PSEN1, and PSEN2 genes are associated with familial forms of early onset Alzheimer's disease.

The aim of this Special Issue of Biomedecines is to present mechanisms involved in neurodegenerative diseases, or to outline therapeutic approaches with their progress and pitfalls.

Dr. Marie-Lise Maddelein
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. Biomedicines 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.

Keywords

  • neurodegenerative diseases
  • neurons
  • mechanism

Published Papers (1 paper)

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

Research

18 pages, 3245 KiB  
Article
Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations
by Khalid Saad Alharbi
Biomedicines 2024, 12(3), 625; https://doi.org/10.3390/biomedicines12030625 - 12 Mar 2024
Viewed by 747
Abstract
Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages [...] Read more.
Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for 15-day. Various behavioral and biochemical parameters including antioxidant levels, oxidative stress, pro-inflammatory markers, mitochondrial enzyme complex, and neurotransmitters were assessed. Europinidin restored biochemical, mitochondrial dysfunction, oxidative stress, neurotransmitter, and pro-inflammatory parameters disrupted by 3-NPA. Here we show that europinidin attenuates 3-NPA-induced neurodegeneration in rat models of HD. Europinidin modulates oxidative stress, enhances antioxidants, restores mitochondrial enzyme complex activity, reduces neuroinflammation, and modulates neurotransmitter levels. Our findings reveal the potential of europinidin as a novel therapeutic agent for the treatment of HD. This study also provides new insights into the molecular mechanisms of europinidin-mediated neuroprotection and may have a beneficial role in the management of neurological diseases. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches)
Show Figures

Figure 1

Back to TopTop