Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Molecular Aspects of the Neurodegenerative Brain Diseases

Special Issue Editors
Special Issue Information
Keywords
Published Papers

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: 10 May 2024 | Viewed by 11225

Share This Special Issue

Special Issue Editor

Dr. Ann-Na Cho

E-Mail Website
Guest Editor

Dementia Research Centre, Macquarie Medical School, Faculty of Medicine Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia
Interests: brain organoid; human stem cell; neuron; tissue engineering

Special Issue Information

Dear Colleagues,

This Special Issue aims to introduce the multiple degrees of the biological environment leading to not only the normal development but also the malfunction of the human brain. To understand brain-related diseases, this Special Issue will focus on the surrounding biomolecular and biochemical information and how it affects the cell population in the brain. More specifically, this issue will cover how to categorize these cues, which type of ligand–receptor interaction is followed, what the outcome of those interplays is, and how a therapeutic approach can be applied to brain-related disorders. Recent advances have led to the development of in vitro resources to model the human brain, such as human stem cell derivates. However, while it is common to concentrate on the cellular components and their responses, in living organisms, the cell population decides its path through consistent stimulation from external information provided by the secretion of molecules by neighboring cells or growth factors and direct contact with scaffold matrices. By applying those multiplex brain environments to the in vitro human brain platform, we can replicate the human brain and ultimately determine the most effective therapeutic approaches.

Dr. Ann-Na Cho
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. 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

brain-related disorder
neurodegenerative disease
biomolecule cue
biochemical cue
molecular mechanism
ligand–receptor interaction
drug response

Published Papers (7 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

19 pages, 18238 KiB

Open AccessArticle

Bisphenol A: Unveiling Its Role in Glioma Progression and Tumor Growth

by Liang Niu, Juan Jia, Hu Yang, Shangyu Liu, Hongyu Wang, Yunji Yan, Qiao Li, Qiang Dong, He Zhang, Guoming Zhao, Junqiang Dai, Guoqiang Yuan and Yawen Pan

Int. J. Mol. Sci. 2024, 25(5), 2504; https://doi.org/10.3390/ijms25052504 - 21 Feb 2024

Viewed by 971

Abstract

Gliomas represent the most common and lethal category of primary brain tumors. Bisphenol A (BPA), a widely recognized endocrine disruptor, has been implicated in the progression of cancer. Despite its established links to various cancers, the association between BPA and glioma progression remains to be clearly defined. This study aimed to shed light on the impact of BPA on glioma cell proliferation and overall tumor progression. Our results demonstrate that BPA significantly accelerates glioma cell proliferation in a time- and dose-dependent manner. Furthermore, BPA has been found to enhance the invasive and migratory capabilities of glioma cells, potentially promoting epithelial–mesenchymal transition (EMT) characteristics within these tumors. Employing bioinformatics approaches, we devised a risk assessment model to gauge the potential glioma hazards associated with BPA exposure. Our comprehensive analysis revealed that BPA not only facilitates glioma invasion and migration but also inhibits apoptotic processes. In summary, our study offers valuable insights into the mechanisms by which BPA may promote tumorigenesis in gliomas, contributing to the understanding of its broader implications in oncology. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

20 pages, 3094 KiB

Open AccessArticle

Blood-Based Transcriptomic Biomarkers Are Predictive of Neurodegeneration Rather Than Alzheimer’s Disease

by Artur Shvetcov, Shannon Thomson, Jessica Spathos, Ann-Na Cho, Heather M. Wilkins, Shea J. Andrews, Fabien Delerue, Timothy A. Couttas, Jasmeen Kaur Issar, Finula Isik, Simranpreet Kaur, Eleanor Drummond, Carol Dobson-Stone, Shantel L. Duffy, Natasha M. Rogers, Daniel Catchpoole, Wendy A. Gold, Russell H. Swerdlow, David A. Brown and Caitlin A. Finney

Int. J. Mol. Sci. 2023, 24(19), 15011; https://doi.org/10.3390/ijms241915011 - 09 Oct 2023

Viewed by 1366

Abstract

Alzheimer’s disease (AD) is a growing global health crisis affecting millions and incurring substantial economic costs. However, clinical diagnosis remains challenging, with misdiagnoses and underdiagnoses being prevalent. There is an increased focus on putative, blood-based biomarkers that may be useful for the diagnosis as well as early detection of AD. In the present study, we used an unbiased combination of machine learning and functional network analyses to identify blood gene biomarker candidates in AD. Using supervised machine learning, we also determined whether these candidates were indeed unique to AD or whether they were indicative of other neurodegenerative diseases, such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Our analyses showed that genes involved in spliceosome assembly, RNA binding, transcription, protein synthesis, mitoribosomes, and NADH dehydrogenase were the best-performing genes for identifying AD patients relative to cognitively healthy controls. This transcriptomic signature, however, was not unique to AD, and subsequent machine learning showed that this signature could also predict PD and ALS relative to controls without neurodegenerative disease. Combined, our results suggest that mRNA from whole blood can indeed be used to screen for patients with neurodegeneration but may be less effective in diagnosing the specific neurodegenerative disease. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

18 pages, 3541 KiB

Open AccessArticle

The UPR Maintains Proteostasis and the Viability and Function of Hippocampal Neurons in Adult Mice

by Pingting Liu, Md Razaul Karim, Ana Covelo, Yuan Yue, Michael K. Lee and Wensheng Lin

Int. J. Mol. Sci. 2023, 24(14), 11542; https://doi.org/10.3390/ijms241411542 - 16 Jul 2023

Cited by 1 | Viewed by 1465

Abstract

The unfolded protein response (UPR), which comprises three branches: PERK, ATF6α, and IRE1, is a major mechanism for maintaining cellular proteostasis. Many studies show that the UPR is a major player in regulating neuron viability and function in various neurodegenerative diseases; however, its role in neurodegeneration is highly controversial. Moreover, while evidence suggests activation of the UPR in neurons under normal conditions, deficiency of individual branches of the UPR has no major effect on brain neurons in animals. It remains unclear whether or how the UPR participates in regulating neuronal proteostasis under normal and disease conditions. To determine the physiological role of the UPR in neurons, we generated mice with double deletion of PERK and ATF6α in neurons. We found that inactivation of PERK and ATF6α in neurons caused lysosomal dysfunction (as evidenced by decreased expression of the V0a1 subunit of v-ATPase and decreased activation of cathepsin D), impairment of autophagic flux (as evidenced by increased ratio of LC3-II/LC3-I and increased p62 level), and accumulation of p-tau and Aβ42 in the hippocampus, and led to impairment of spatial memory, impairment of hippocampal LTP, and hippocampal degeneration in adult mice. These results suggest that the UPR is required for maintaining neuronal proteostasis (particularly tau and Aβ homeostasis) and the viability and function of neurons in the hippocampus of adult mice. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

18 pages, 4768 KiB

Open AccessArticle

Comparison of Monoamine Oxidase-A, Aβ Plaques, Tau, and Translocator Protein Levels in Postmortem Human Alzheimer’s Disease Brain

by Amina U. Syed, Christopher Liang, Krystal K. Patel, Rommani Mondal, Vallabhi M. Kamalia, Taylor R. Moran, Shamiha T. Ahmed and Jogeshwar Mukherjee

Int. J. Mol. Sci. 2023, 24(13), 10808; https://doi.org/10.3390/ijms241310808 - 28 Jun 2023

Cited by 4 | Viewed by 1287

Abstract

Increased monoamine oxidase-A (MAO-A) activity in Alzheimer’s disease (AD) may be detrimental to the point of neurodegeneration. To assess MAO-A activity in AD, we compared four biomarkers, Aβ plaques, tau, translocator protein (TSPO), and MAO-A in postmortem AD. Radiotracers were [¹⁸F]FAZIN3 for MAO-A, [¹⁸F]flotaza and [¹²⁵I]IBETA for Aβ plaques, [^124/125I]IPPI for tau, and [¹⁸F]FEPPA for TSPO imaging. Brain sections of the anterior cingulate (AC; gray matter GM) and corpus callosum (CC; white matter WM) from cognitively normal control (CN, n = 6) and AD (n = 6) subjects were imaged using autoradiography and immunostaining. Using competition with clorgyline and (R)-deprenyl, the binding of [¹⁸F]FAZIN3 was confirmed to be selective to MAO-A levels in the AD brain sections. Increases in MAO-A, Aβ plaque, tau, and TSPO activity were found in the AD brains compared to the control brains. The [¹⁸F]FAZIN3 ratio in AD GM versus CN GM was 2.80, suggesting a 180% increase in MAO-A activity. Using GM-to-WM ratios of AD versus CN, a >50% increase in MAO-A activity was observed (AD/CN = 1.58). Linear positive correlations of [¹⁸F]FAZIN3 with [¹⁸F]flotaza, [¹²⁵I]IBETA, and [¹²⁵I]IPPI were measured and suggested an increase in MAO-A activity with increases in Aβ plaques and tau activity. Our results support the finding that MAO-A activity is elevated in the anterior cingulate cortex in AD and thus may provide a new biomarker for AD in this brain region. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

Review

Jump to: Research

20 pages, 2284 KiB

Open AccessReview

The Importance of Complement-Mediated Immune Signaling in Alzheimer’s Disease Pathogenesis

by André F. Batista, Khyrul A. Khan, Maria-Tzousi Papavergi and Cynthia A. Lemere

Int. J. Mol. Sci. 2024, 25(2), 817; https://doi.org/10.3390/ijms25020817 - 09 Jan 2024

Cited by 2 | Viewed by 1886

Abstract

As an essential component of our innate immune system, the complement system is responsible for our defense against pathogens. The complement cascade has complex roles in the central nervous system (CNS), most of what we know about it stems from its role in brain development. However, in recent years, numerous reports have implicated the classical complement cascade in both brain development and decline. More specifically, complement dysfunction has been implicated in neurodegenerative disorders, such as Alzheimer’s disease (AD), which is the most common form of dementia. Synapse loss is one of the main pathological hallmarks of AD and correlates with memory impairment. Throughout the course of AD progression, synapses are tagged with complement proteins and are consequently removed by microglia that express complement receptors. Notably, astrocytes are also capable of secreting signals that induce the expression of complement proteins in the CNS. Both astrocytes and microglia are implicated in neuroinflammation, another hallmark of AD pathogenesis. In this review, we provide an overview of previously known and newly established roles for the complement cascade in the CNS and we explore how complement interactions with microglia, astrocytes, and other risk factors such as TREM2 and ApoE4 modulate the processes of neurodegeneration in both amyloid and tau models of AD. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

19 pages, 3048 KiB

Open AccessReview

Potential Role of Antibodies against Aquaporin-1 in Patients with Central Nervous System Demyelination

by Maria Pechlivanidou, Konstantina Xenou, Dimitrios Tzanetakos, Emmanuel Koutsos, Christos Stergiou, Elisabeth Andreadou, Konstantinos Voumvourakis, Sotirios Giannopoulos, Constantinos Kilidireas, Erdem Tüzün, Georgios Tsivgoulis, Socrates Tzartos and John Tzartos

Int. J. Mol. Sci. 2023, 24(16), 12982; https://doi.org/10.3390/ijms241612982 - 19 Aug 2023

Viewed by 1717

Abstract

Aquaporins (AQPs; AQP0–AQP12) are water channels expressed in many and diverse cell types, participating in various functions of cells, tissues, and systems, including the central nervous system (CNS). AQP dysfunction and autoimmunity to AQPs are implicated in several diseases. The best-known example of autoimmunity against AQPs concerns the antibodies to AQP4 which are involved in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD), an autoimmune astrocytopathy, causing also CNS demyelination. The present review focuses on the discovery and the potential role of antibodies against AQP1 in the CNS, and their potential involvement in the pathophysiology of NMOSD. We describe (a) the several techniques developed for the detection of the AQP1-antibodies, with emphasis on methods that specifically identify antibodies targeting the extracellular domain of AQP1, i.e., those of potential pathogenic role, and (b) the available evidence supporting the pathogenic relevance of AQP1-antibodies in the NMOSD phenotype. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Figure 1

21 pages, 1032 KiB

Open AccessReview

Molecular Aspects of a Diet as a New Pathway in the Prevention and Treatment of Alzheimer’s Disease

by Julia Doroszkiewicz, Jan Mroczko, Piotr Rutkowski and Barbara Mroczko

Int. J. Mol. Sci. 2023, 24(13), 10751; https://doi.org/10.3390/ijms241310751 - 28 Jun 2023

Viewed by 1839

Abstract

Alzheimer’s disease is the most common cause of dementia in the world. Lack of an established pathology makes it difficult to develop suitable approaches and treatment for the disease. Besides known hallmarks, including amyloid β peptides cumulating in plaques and hyperphosphorylated tau forming NFTs, inflammation also plays an important role, with known connections to the diet. In AD, adhering to reasonable nutrition according to age-related principles is recommended. The diet should be high in neuroprotective foods, such as polyunsaturated fatty acids, antioxidants, and B vitamins. In addition, foods capable of rising BDNF should be considered because of the known profitable results of this molecule in AD. Adhering to beneficial diets might result in improvements in memory, cognition, and biomarkers and might even reduce the risk of developing AD. In this review, we discuss the effects of various diets, foods, and nutrients on brain health and possible connections to Alzheimer’s disease. Full article

(This article belongs to the Special Issue Molecular Aspects of the Neurodegenerative Brain Diseases)

► Show Figures

Journal Menu

Journal Browser

Molecular Aspects of the Neurodegenerative Brain Diseases

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (7 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI