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Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition
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Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 1970

Special Issue Editors

Dr. Zhidong Zhou

E-Mail Website
Guest Editor
Translational Therapeutics Laboratory, Duke-NUS Graduate Medical School, NBD, Level 6, 8 College Road, Singapore 169857, Singapore
Interests: Biomarkers; therapeutic targets and compounds for Parkinson's disease and other neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Alexandre Hiroaki Kihara

E-Mail Website
Guest Editor
Centro de Matemática, Computação e Cognição, Universidade Federal do ABC, São Bernardo do Campo, Santo André, Brazil
Interests: stem cells; sci; genome; CRISPR associated endonuclease Cas9; gene editing; electrocorticography; high frequency oscillation; seizures
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are a group of heterogeneous disorders characterized with progressive neuron vulnerability and even neuron demise in the brain or peripheral nervous system, which are listed within the leading causes for human death. Among various neurodegenerative conditions, Alzheimer's disease and Parkinson's disease (PD) are the most common neurodegenerative disorders. With the aging of our population, the prevalence of neurodegenerative diseases increases significantly, posing serious healthy and economic challenges all around the world. Although oxidative stress, protein aggregation, mitochondria impairment, and neuroinflammation are relevant to neurodegeneration, the disease pathogenesis are not fully understood and no therapy available for these degenerative disorders. Recently, cell therapies using human cell derived dopamine neurons to replace lost neurons in PD patient brains show promise and the first human clinical trial of transplantation of induced pluripotent stem cells derived human dopamine progenitors is under investigation in the Center for iPS Cell Research and Application (CiRA), Kyoto University, which brings hopes to patients with PD and other degenerative diseases.

The aim of this Special Issue is to discuss the disease pathogenesis and new therapeutic agents or therapeutic strategies to protect or alleviate neurodegeneration in human neurodegenerative disorders.

Dr. Zhidong Zhou
Dr. Alexandre Hiroaki Kihara
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurodegeneration
  • neurodegenerative diseases
  • protein aggregation
  • pathogenesis
  • therapy
  • mitochondria
  • neuroinflammation
  • oxidative stress
  • cell therapy
  • clinical trial 

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Published Papers (2 papers)

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Research

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22 pages, 6840 KiB  
Article
Noradrenaline Protects Human Microglial Cells (HMC3) Against Apoptosis and DNA Damage Induced by LPS and Aβ1-42 Aggregates In Vitro
by Julia Barczuk, Grzegorz Galita, Natalia Siwecka, Michał Golberg, Kamil Saramowicz, Zuzanna Granek, Wojciech Wiese, Ireneusz Majsterek and Wioletta Rozpędek-Kamińska
Int. J. Mol. Sci. 2024, 25(21), 11399; https://doi.org/10.3390/ijms252111399 - 23 Oct 2024
Viewed by 704
Abstract
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, characterized by the accumulation of amyloid-beta (Aβ) plaques and neuroinflammation. This study investigates the protective effects of noradrenaline (NA) on human microglial cells exposed to lipopolysaccharides (LPS) and Aβ aggregates—major contributors to inflammation and [...] Read more.
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, characterized by the accumulation of amyloid-beta (Aβ) plaques and neuroinflammation. This study investigates the protective effects of noradrenaline (NA) on human microglial cells exposed to lipopolysaccharides (LPS) and Aβ aggregates—major contributors to inflammation and cellular damage in AD. The reduced Aβ aggregation in the HMC3 human microglial cells co-treated with Aβ and NA was confirmed by thioflavin T (ThT) assay, fluorescent ThT staining, and immunocytochemistry (ICC). The significantly increased viability of HMC3 cells after 48 h of incubation with NA at 50 µM, 25 µM, and 10 µM, exposed to IC50 LPS and IC50 Aβ, was confirmed by XTT and LDH assays. Moreover, we found that NA treatment at 25 μM and 50 μM concentrations in HMC3 cells exposed to IC50 LPS or IC50 Aβ results in an increased proliferation of HMC3 cells, their return to normal morphology, decreased levels of DNA damage, reduced caspase-3 activity, decreased expression of pro-apoptotic DDIT3 and BAX, and increased expression of anti-apoptotic BCL-2 genes and proteins, leading to enhanced cell survival, when compared to that of the HMC3 cells treated only with IC50 LPS or IC50 Aβ. Furthermore, we showed that NA induces the degradation of both extracellular and intracellular Aβ deposits and downregulates hypoxia-inducible factor 1α (HIF-1α), which is linked to impaired Aβ clearance and AD progression. These findings indicate that NA holds promise as a therapeutic target to address microglial dysfunction and potentially slow the progression of AD. Its neuroprotective effects, particularly in reducing inflammation and regulating microglial activity, warrant further investigation into its broader role in mitigating neuroinflammation and preserving microglial function in AD. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition)
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Review

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27 pages, 1649 KiB  
Review
Train and Reprogram Your Brain: Effects of Physical Exercise at Different Stages of Life on Brain Functions Saved in Epigenetic Modifications
by Magdalena Kukla-Bartoszek and Katarzyna Głombik
Int. J. Mol. Sci. 2024, 25(22), 12043; https://doi.org/10.3390/ijms252212043 - 9 Nov 2024
Viewed by 877
Abstract
Multiple studies have demonstrated the significant effects of physical exercise on brain plasticity, the enhancement of memory and cognition, and mood improvement. Although the beneficial impact of exercise on brain functions and mental health is well established, the exact mechanisms underlying this phenomenon [...] Read more.
Multiple studies have demonstrated the significant effects of physical exercise on brain plasticity, the enhancement of memory and cognition, and mood improvement. Although the beneficial impact of exercise on brain functions and mental health is well established, the exact mechanisms underlying this phenomenon are currently under thorough investigation. Several hypotheses have emerged suggesting various possible mechanisms, including the effects of hormones, neurotrophins, neurotransmitters, and more recently also other compounds such as lactate or irisin, which are released under the exercise circumstances and act both locally or/and on distant tissues, triggering systemic body reactions. Nevertheless, none of these actually explain the long-lasting effect of exercise, which can persist for years or even be passed on to subsequent generations. It is believed that these long-lasting effects are mediated through epigenetic modifications, influencing the expression of particular genes and the translation and modification of specific proteins. This review explores the impact of regular physical exercise on brain function and brain plasticity and the associated occurrence of epigenetic modifications. It examines how these changes contribute to the prevention and treatment of neuropsychiatric and neurological disorders, as well as their influence on the natural aging process and mental health. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition)
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