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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 September 2025 | Viewed by 10199

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

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Keywords

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

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Published Papers (4 papers)

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Research

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11 pages, 1321 KiB  
Article
Possible Impact of Peripheral Inflammatory Factors and Interleukin-1β (IL-1β) on Cognitive Functioning in Progressive Supranuclear Palsy–Richardson Syndrome (PSP-RS) and Progressive Supranuclear Palsy–Predominant Parkinsonism (PSP-P)
by Patryk Chunowski, Dagmara Otto-Ślusarczyk, Karolina Duszyńska-Wąs, Agnieszka Drzewińska, Andrzej Załęski, Natalia Madetko-Alster, Alicja Wiercińska-Drapało, Marta Struga and Piotr Alster
Int. J. Mol. Sci. 2024, 25(23), 13211; https://doi.org/10.3390/ijms252313211 - 9 Dec 2024
Cited by 2 | Viewed by 863
Abstract
Progressive supranuclear palsy (PSP) is a tauopathic atypical parkinsonian syndrome. Recent studies suggest that inflammation may play a role in PSP pathogenesis, highlighting markers like the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and cytokines such as IL-1β and IL-6. This study aimed to [...] Read more.
Progressive supranuclear palsy (PSP) is a tauopathic atypical parkinsonian syndrome. Recent studies suggest that inflammation may play a role in PSP pathogenesis, highlighting markers like the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and cytokines such as IL-1β and IL-6. This study aimed to assess the relationship between peripheral inflammatory markers and psychological abnormalities in PSP-RS and PSP-P patients. The study included 24 participants: 12 with PSP-RS, 12 with PSP-P, and 12 controls. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA); however, the executive functions were evaluated using the Frontal Assessment Battery (FAB), while inflammatory markers such as IL-1β, IL6, NLR, and PLR were measured. The parameter correlation was executed using Spearman’s correlation (rs). The analysis revealed significant negative correlations between NLR and MoCA (rs = −0.48), as well as between PLR and MoCA (rs = −0.60). The negative correlation between IL-1β and MoCA was statistically significant but relatively weak. This study highlights the relevance of inflammatory markers such as NLR and PLR in reflecting cognitive decline in PSP patients, with IL-1β potentially playing a protective role in cognitive function. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition)
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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 1772
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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26 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
Cited by 1 | Viewed by 4978
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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Other

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10 pages, 274 KiB  
Commentary
The α-Synuclein Seeding Amplification Assay for Parkinson’s Disease
by Ling-Xiao Yi, Eng King Tan and Zhi Dong Zhou
Int. J. Mol. Sci. 2025, 26(1), 389; https://doi.org/10.3390/ijms26010389 - 4 Jan 2025
Viewed by 1876
Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world. Currently, PD is incurable, and the diagnosis of PD mainly relies on clinical manifestations. The central pathological event in PD is the abnormal aggregation and deposition of misfolded α-synuclein (α-Syn) [...] Read more.
Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world. Currently, PD is incurable, and the diagnosis of PD mainly relies on clinical manifestations. The central pathological event in PD is the abnormal aggregation and deposition of misfolded α-synuclein (α-Syn) protein aggregates in the Lewy body (LB) in affected brain areas. Behaving as a prion-like seeding, the misfolded α-syn protein can induce and facilitate the aggregation of native unfolded α-Syn protein to aggravate α-Syn protein aggregation, leading to PD progression. Recently, in a blood-based α-Syn seeding amplification assay (SAA), Kluge et al. identified pathological α-Syn seeding activity in PD patients with Parkin (PRKN) gene variants. Additionally, pathological α-syn seeding activity was also identified in sporadic PD and PD patients with Leucine-rich repeat kinase 2 (LRRK2) or glucocerebrosidase (GBA) gene variants. Principally, the α-Syn SAA can be used to detect pathological α-Syn seeding activity, which will significantly enhance PD diagnosis, progression monitoring, prognosis prediction, and anti-PD therapy. The significance and future strategies of α-Syn SAA protocol are highlighted and proposed, whereas challenges and limitations of the assay are discussed. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapies, 3rd Edition)
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