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Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders, 2nd 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 August 2025 | Viewed by 4277

Special Issue Editor

Dr. Yasemin M. Akay

E-Mail Website
Guest Editor
Department of Biomedical Engineering, University of Houston, Houston, TX 77204-5060, USA
Interests: coronary artery disease; stent; noninvasive monitoring; nonlinear dynamics analysis; approximate entropy; 3D co-culture; glioblastoma; astrocytes; tumor microenvironment; PEGDA; addiction; cancer research; data science in medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The increase in patients with dementia and motor dysfunction due to the global aging population is a significant social problem. No fundamental treatment for these cognitive-motor disorders has yet been developed. Therefore, understanding the etiology of aging-related disorders and exploring unique therapeutic targets to develop total therapies are urgent issues. Accordingly, comprehending the degeneration of brain function with aging is essential. To this end, it is necessary to distinguish the molecular mechanisms required to maintain neuronal homeostasis and the characteristics of pathogenic proteins. Thus, this Special Issue focuses on the pathogenic mechanism involved in the etiology of neurodegeneration, which includes Alzheimer's disease (AD), Parkinson's (PD), and dementia with Lewy bodies (DLB), demonstrating the physiological significance of the pathogenic proteins. We also focus on the disease-related biomarkers associated with the age- and disease-induced loss of neuronal homeostasis. The goal of this Special Issue is to subsequently improve our understanding of aging-related neurodegenerative disorders and to make breakthroughs in the prediction of pathogenesis and the development of fundamental treatments for these diseases.

Potential topics include, but are not limited to: Parkinson's disease (PD), Dementia with Lewy bodies (DLB), Alzheimer's disease (AD), pathogenic proteins in the above diseases, biomarkers for AD, PD, and DLB, therapeutic targets and drugs for AD, PD, and DLB, and reviews and future perspectives on the above topics.

Due to the success of the first edition of this Special Issue, we would like to add more results and new insights from recent research projects.

https://www.mdpi.com/journal/ijms/special_issues/3POPNIW1Y3

Dr. Yasemin M. Akay
Guest Editor

Manuscript Submission Information

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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

  • Parkinson's disease
  • dementia with Lewy bodies
  • Alzheimer's disease
  • pathogenic protein
  • biomarker
  • therapeutic target
  • drug

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Related Special Issue

Published Papers (3 papers)

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Research

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18 pages, 12353 KiB  
Article
Oroxylum indicum (L.) Leaf Extract Attenuates β-Amyloid-Induced Neurotoxicity in SH-SY5Y Cells
by Nut Palachai, Benjaporn Buranrat, Parinya Noisa and Nootchanat Mairuae
Int. J. Mol. Sci. 2025, 26(7), 2917; https://doi.org/10.3390/ijms26072917 - 23 Mar 2025
Viewed by 542
Abstract
Alzheimer’s disease (AD) is characterized by the presence of amyloid-beta (Aβ) plaques, which trigger oxidative stress and neuronal cell death. The present study investigated the neuroprotective effects of Oroxylum indicum (L.) leaf (OIL) extract against Aβ-induced oxidative stress and cellular damage in SH-SY5Y [...] Read more.
Alzheimer’s disease (AD) is characterized by the presence of amyloid-beta (Aβ) plaques, which trigger oxidative stress and neuronal cell death. The present study investigated the neuroprotective effects of Oroxylum indicum (L.) leaf (OIL) extract against Aβ-induced oxidative stress and cellular damage in SH-SY5Y cells. The cells were treated with OIL extract with and without Aβ25−35, and their viability was investigated. Moreover, the mechanism of action of OIL was assessed by determining caspase-3 levels, reactive oxygen species (ROS) and malondialdehyde (MDA) levels, enzymatic activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), extracellular signal-regulated kinase 1 and 2 (ERK1/2), and cAMP-responsive element-binding protein (CREB), and expression of B-cell lymphoma-2 (Bcl-2) proteins. The results indicated that OIL reduced Aβ-induced neurotoxicity in a concentration-dependent manner, improving cell viability, reducing ROS levels and MDA production, increasing antioxidant enzyme activity of CAT, SOD, and GSH-Px, and decreasing caspase-3 expression. In addition, OIL enhanced phosphorylation of Akt, ERK1/2, and CREB and upregulated Bcl-2 protein expression. High-performance liquid chromatography (HPLC) analysis identified oroxylin A, baicalein, and chrysin as the major phenolic constituents of the OIL extract. The findings suggest that the extract holds promise as a therapeutic intervention against Aβ-induced neurotoxicity, offering potential implications for the treatment of AD. Further studies are needed to investigate the activity of OIL in primary neurons or in vivo. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders, 2nd Edition)
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34 pages, 3163 KiB  
Article
Resting-State EEG Alpha Rhythms Are Related to CSF Tau Biomarkers in Prodromal Alzheimer’s Disease
by Claudio Del Percio, Roberta Lizio, Susanna Lopez, Giuseppe Noce, Matteo Carpi, Dharmendra Jakhar, Andrea Soricelli, Marco Salvatore, Görsev Yener, Bahar Güntekin, Federico Massa, Dario Arnaldi, Francesco Famà, Matteo Pardini, Raffaele Ferri, Filippo Carducci, Bartolo Lanuzza, Fabrizio Stocchi, Laura Vacca, Chiara Coletti, Moira Marizzoni, John Paul Taylor, Lutfu Hanoğlu, Nesrin Helvacı Yılmaz, İlayda Kıyı, Yağmur Özbek-İşbitiren, Anita D’Anselmo, Laura Bonanni, Roberta Biundo, Fabrizia D’Antonio, Giuseppe Bruno, Angelo Antonini, Franco Giubilei, Lucia Farotti, Lucilla Parnetti, Giovanni B. Frisoni and Claudio Babiloniadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2025, 26(1), 356; https://doi.org/10.3390/ijms26010356 - 3 Jan 2025
Viewed by 1746
Abstract
Patients with mild cognitive impairment due to Alzheimer’s disease (ADMCI) typically show abnormally high delta (<4 Hz) and low alpha (8–12 Hz) rhythms measured from resting-state eyes-closed electroencephalographic (rsEEG) activity. Here, we hypothesized that the abnormalities in rsEEG activity may be greater in [...] Read more.
Patients with mild cognitive impairment due to Alzheimer’s disease (ADMCI) typically show abnormally high delta (<4 Hz) and low alpha (8–12 Hz) rhythms measured from resting-state eyes-closed electroencephalographic (rsEEG) activity. Here, we hypothesized that the abnormalities in rsEEG activity may be greater in ADMCI patients than in those with MCI not due to AD (noADMCI). Furthermore, they may be associated with the diagnostic cerebrospinal fluid (CSF) amyloid–tau biomarkers in ADMCI patients. An international database provided clinical–demographic–rsEEG datasets for cognitively unimpaired older (Healthy; N = 45), ADMCI (N = 70), and noADMCI (N = 45) participants. The rsEEG rhythms spanned individual delta, theta, and alpha frequency bands. The eLORETA freeware estimated cortical rsEEG sources. Posterior rsEEG alpha source activities were reduced in the ADMCI group compared not only to the Healthy group but also to the noADMCI group (p < 0.001). Negative associations between the CSF phospho-tau and total tau levels and posterior rsEEG alpha source activities were observed in the ADMCI group (p < 0.001), whereas those with CSF amyloid beta 42 levels were marginal. These results suggest that neurophysiological brain neural oscillatory synchronization mechanisms regulating cortical arousal and vigilance through rsEEG alpha rhythms are mainly affected by brain tauopathy in ADMCI patients. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders, 2nd Edition)
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Review

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33 pages, 1399 KiB  
Review
An Update on Neuroaging on Earth and in Spaceflight
by Nik V. Kuznetsov, Yauhen Statsenko and Milos Ljubisavljevic
Int. J. Mol. Sci. 2025, 26(4), 1738; https://doi.org/10.3390/ijms26041738 - 18 Feb 2025
Viewed by 1167
Abstract
Over 400 articles on the pathophysiology of brain aging, neuroaging, and neurodegeneration were reviewed, with a focus on epigenetic mechanisms and numerous non-coding RNAs. In particular, this review the accent is on microRNAs, the discovery of whose pivotal role in gene regulation was [...] Read more.
Over 400 articles on the pathophysiology of brain aging, neuroaging, and neurodegeneration were reviewed, with a focus on epigenetic mechanisms and numerous non-coding RNAs. In particular, this review the accent is on microRNAs, the discovery of whose pivotal role in gene regulation was recognized by the 2024 Nobel Prize in Physiology or Medicine. Aging is not a gradual process that can be easily modeled and described. Instead, multiple temporal processes occur during aging, and they can lead to mosaic changes that are not uniform in pace. The rate of change depends on a combination of external and internal factors and can be boosted in accelerated aging. The rate can decrease in decelerated aging due to individual structural and functional reserves created by cognitive, physical training, or pharmacological interventions. Neuroaging can be caused by genetic changes, epigenetic modifications, oxidative stress, inflammation, lifestyle, and environmental factors, which are especially noticeable in space environments where adaptive changes can trigger aging-like processes. Numerous candidate molecular biomarkers specific to neuroaging need to be validated to develop diagnostics and countermeasures. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders, 2nd Edition)
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