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Neuropathology: From Molecular Mechanisms to Therapeutic Solutions

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 9730

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Special Issue Editors

Dr. Wenqiang Fan

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Guest Editor

Neuroscience Therapeutic Area, UCB Biopharma SPRL, 1420 Braine-l'Alleud, Belgium
Interests: neuroinflammation; neurodevelopment; neurogenesis; neurodegenerative diseases

Dr. Xingping Qin

E-Mail Website
Guest Editor

Harvard School of Public Health, Harvard University, Boston, MA 02115, USA
Interests: cerebral ischemia; cerebral hemorrhage; glioblastoma; medulloblastoma; apoptosis

Special Issue Information

Dear Colleagues,

In recent years, there has been a dramatic increase in the number of patients with neurological diseases including neurodegenerative diseases. This has exerted a major societal and financial burden worldwide, and these diseases remain a major cause of disability. Many neurological disorders strike primarily in mid- to late life; their incidence is expected to soar as the population ages. By 2030, as many as one in five Americans will be over the age 65, and more than 12 million Americans will suffer from neurological disorders. Promising studies have been made to understand the molecular mechanisms of disease progression and detailed insights into potential therapeutic solutions. This Special Issue focuses on new and fast-developing knowledge on the disease mechanisms and therapeutic approaches for neurological diseases.

This Special Issue intends to highlight the advances in our understanding of the molecular mechanisms of neurological disorders and potential therapeutic solutions to slow down or prevent the progression of the diseases. With this Special Issue, we hope to provide a comprehensive overview from molecular mechanisms to therapeutic solutions of neurological diseases for the broad readership of the journal.

Dr. Wenqiang Fan
Dr. Xingping Qin
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.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 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

molecular neuropathology
pathogenesis of nervous system disorders
CNS tumors
neuroinflammation
multiple sclerosis
neurodegenerative diseases
dementias
Alzheimer disease
synucleinopathies
tauopathies
glioblastoma
medulloblastoma

Published Papers (6 papers)

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Research

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17 pages, 5617 KiB

Open AccessArticle

Neuroprotective Effects of Water Extract from Brown Algae Petalonia binghamiae in an Experimental Model of Focal Cerebral Ischemia In Vitro and In Vivo

by Sun Ho Eom, Geum-Lan Hong, Hyun Bae Kang, Nam-Seob Lee, Do Kyung Kim, Young Gil Jeong, Chun-Sung Kim, Yung Choon Yoo, Bong Ho Lee, Ju-Young Jung, Dong-Sub Kim and Seung Yun Han

Curr. Issues Mol. Biol. 2023, 45(10), 8427-8443; https://doi.org/10.3390/cimb45100531 - 17 Oct 2023

Cited by 1 | Viewed by 1112

Abstract

Focal cerebral ischemia (fCI) can result in brain injury and sensorimotor deficits. Brown algae are currently garnering scientific attention as potential therapeutic candidates for fCI. This study investigated the therapeutic effects of the hot water extract of Petalonia binghamiae (wPB), a brown alga, in in vitro and in vivo models of fCI. The neuroprotective efficacy of wPB was evaluated in an in vitro excitotoxicity model established using HT-22 cells challenged with glutamate. Afterward, C57/BL6 mice were administered wPB for 7 days (10 or 100 mg/kg, intragastric) and subjected to middle cerebral artery occlusion and reperfusion (MCAO/R) operation, which was used as an in vivo fCI model. wPB co-incubation significantly inhibited cell death, oxidative stress, and apoptosis, as well as stimulated the expression of heme oxygenase-1 (HO-1), an antioxidant enzyme, and the nuclear translocation of its upstream regulator, nuclear factor erythroid 2-related factor 2 (Nrf2) in HT-22 cells challenged with glutamate-induced excitotoxicity. Pretreatment with either dose of wPB significantly attenuated infarction volume, neuronal death, and sensorimotor deficits in an in vivo fCI model. Furthermore, the attenuation of oxidative stress and apoptosis in the ischemic lesion accompanied the wPB-associated protection. This study suggests that wPB can counteract fCI via an antioxidative effect, upregulating the Nrf2/HO-1 pathway. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

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17 pages, 7972 KiB

Open AccessArticle

Involvement of Glycogen Synthase Kinase 3β (GSK3β) in Formation of Phosphorylated Tau and Death of Retinal Ganglion Cells of Rats Caused by Optic Nerve Crush

by Yurie Fukiyama, Takahisa Hirokawa, Shinji Takai, Teruyo Kida and Hidehiro Oku

Curr. Issues Mol. Biol. 2023, 45(9), 6941-6957; https://doi.org/10.3390/cimb45090438 - 22 Aug 2023

Viewed by 892

Abstract

Tauopathy is a neurodegenerative condition associated with oligomeric tau formation through abnormal phosphorylation. We previously showed that tauopathy is involved in death of retinal ganglion cells (RGCs) after optic nerve crush (ONC). It has been proposed that glycogen synthase kinase 3β (GSK3β) is involved in the hyperphosphorylation of tau in Alzheimer’s disease. To determine the roles of GSK3β in tauopathy-related death of RGCs, lithium chloride (LiCl), a GSK3β inhibitor, was injected intravitreally just after ONC. The neuroprotective effects of LiCl were determined by counting Tuj-1-stained RGCs on day 7. Changes of phosphorylated (ser 396) tau in the retina were determined by Simple Western analysis (WES) on day 3. Retinal GSK3β levels were determined by immunohistochemistry (IHC) and an ELISA. There was a 1.9- and 2.1-fold increase in the levels of phosphorylated tau monomers and dimers on day 3 after ONC. LiCl significantly suppressed the increase in the levels of phosphorylated tau induced by ONC. GSK3β was mainly present in somas of RGCs, and ELISA showed that retinal levels increased to 2.0-fold on day 7. IHC showed that the GSK3β expression increased over time and remained in RGCs that were poorly stained by Tuj-1. The GSK3β and tau expression was colocalized in RGCs. The number of RGCs decreased from 1881 ± 188 (sham control) to 1150 ± 192 cells/mm² on day 7, and LiCl preserved the levels at 1548 ± 173 cells/mm². Accordingly, GSK3β may be a promising target for some optic nerve injuries. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

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15 pages, 2750 KiB

Open AccessArticle

Neural Differentiation of Induced Pluripotent Stem Cells for a Xenogeneic Material-Free 3D Neurological Disease Model Neurulation from Pluripotent Cells Using a Human Hydrogel

by Luis Sebastian Alexis Valerio, Frederick Robert Carrick, Lina Bedoya, Sandeep Sreerama and Kiminobu Sugaya

Curr. Issues Mol. Biol. 2023, 45(6), 4574-4588; https://doi.org/10.3390/cimb45060290 - 25 May 2023

Viewed by 2485

Abstract

Alzheimer’s Disease (AD) is characterized by synapse and neuronal loss and the accumulation of neurofibrillary tangles and Amyloid β plaques. Despite significant research efforts to understand the late stages of the disease, its etiology remains largely unknown. This is in part because of the imprecise AD models in current use. In addition, little attention has been paid to neural stem cells (NSC), which are the cells responsible for the development and maintenance of brain tissue during an individual’s lifespan. Thus, an in vitro 3D human brain tissue model using induced pluripotent stem (iPS) cell-derived neural cells in human physiological conditions may be an excellent alternative to standard models to investigate AD pathology. Following the differentiation process mimicking development, iPS cells can be turned into NSCs and, ultimately, neural cells. During differentiation, the traditionally used xenogeneic products may alter the cells’ physiology and prevent accurate disease pathology modeling. Hence, establishing a xenogeneic material-free cell culture and differentiation protocol is essential. This study investigated the differentiation of iPS cells to neural cells using a novel extracellular matrix derived from human platelet lysates (PL Matrix). We compared the stemness properties and differentiation efficacies of iPS cells in a PL matrix against those in a conventional 3D scaffold made of an oncogenic murine-matrix. Using well-defined conditions without xenogeneic material, we successfully expanded and differentiated iPS cells into NSCs via dual-SMAD inhibition, which regulates the BMP and TGF signaling cascades in a manner closer to human conditions. This in vitro, 3D, xenogeneic-free scaffold will enhance the quality of disease modeling for neurodegenerative disease research, and the knowledge produced could be used in developing more effective translational medicine. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

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11 pages, 289 KiB

Open AccessArticle

Serum Growth Factors in Schizophrenia Patients

by Anastasiia S. Boiko, Irina A. Mednova, Elena G. Kornetova, Nikolay A. Bokhan and Svetlana A. Ivanova

Curr. Issues Mol. Biol. 2023, 45(4), 3291-3301; https://doi.org/10.3390/cimb45040215 - 07 Apr 2023

Viewed by 1213

Abstract

Some hypotheses include schizophrenia as a neurodevelopmental disorder, which indicates a special role in growth factors and neuroglia in the development of schizophrenia symptoms. Growth factors are cytokine molecules that play an important role in the regulation of tissue nucleation, cell development, survival, and migration of all tissues in organisms, including the brain and nervous system. The aim of the study was to determine the serum concentration of six growth factors (EGF, VEGF, FGF-2, TGF-α, PDGF-AA, PDGF-AB/BB) in schizophrenia patients and to identify the correlations with clinical characteristics. After signing an informed consent form, 236 schizophrenia patients (F20 according to the ICD-10) and 102 healthy people were recruited in the study. In patients with schizophrenia, we observed a significant elevation in the TGF-α and PDGF-AA serum levels. The duration of schizophrenia was significantly positively correlated with the FGF-2 level. The PANSS total score had a positive correlation with the FGF-2 level and a negative correlation with the TGF-α level. Our results and literature indicate the involvement of growth factors in the mechanisms of development of schizophrenia. Combined biomarker screening seems to be necessary to improve diagnosis and clinical follow-up of patients with severe mental illnesses. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

Review

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18 pages, 1117 KiB

Open AccessReview

The Deficits of Insulin Signal in Alzheimer’s Disease and the Mechanisms of Vanadium Compounds in Curing AD

by Jinyi Yao, Zhijun He, Guanying You, Qiong Liu and Nan Li

Curr. Issues Mol. Biol. 2023, 45(8), 6365-6382; https://doi.org/10.3390/cimb45080402 - 31 Jul 2023

Cited by 1 | Viewed by 1159

Abstract

Vanadium is a well-known essential trace element, which usually exists in oxidation states in the form of a vanadate cation intracellularly. The pharmacological study of vanadium began with the discovery of its unexpected inhibitory effect on ATPase. Thereafter, its protective effects on β cells and its ability in glucose metabolism regulation were observed from the vanadium compound, leading to the application of vanadium compounds in clinical trials for curing diabetes. Alzheimer’s disease (AD) is the most common dementia disease in elderly people. However, there are still no efficient agents for treating AD safely to date. This is mainly because of the complexity of the pathology, which is characterized by senile plaques composed of the amyloid-beta (Aβ) protein in the parenchyma of the brain and the neurofibrillary tangles (NFTs), which are derived from the hyperphosphorylated tau protein in the neurocyte, along with mitochondrial damage, and eventually the central nervous system (CNS) atrophy. AD was also illustrated as type-3 diabetes because of the observations of insulin deficiency and the high level of glucose in cerebrospinal fluid (CSF), as well as the impaired insulin signaling in the brain. In this review, we summarize the advances in applicating the vanadium compound to AD treatment in experimental research and point out the limitations of the current study using vanadium compounds in AD treatment. We hope this will help future studies in this field. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

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20 pages, 1045 KiB

Open AccessReview

Specific Features of Focal Cortical Dysplasia in Tuberous Sclerosis Complex

by Ekaterina Bychkova, Marina Dorofeeva, Aleksandr Levov, Alexey Kislyakov, Kristina Karandasheva, Vladimir Strelnikov and Kirill Anoshkin

Curr. Issues Mol. Biol. 2023, 45(5), 3977-3996; https://doi.org/10.3390/cimb45050254 - 03 May 2023

Viewed by 2189

Abstract

Patients with tuberous sclerosis complex present with cognitive, behavioral, and psychiatric impairments, such as intellectual disabilities, autism spectrum disorders, and drug-resistant epilepsy. It has been shown that these disorders are associated with the presence of cortical tubers. Tuberous sclerosis complex results from inactivating mutations in the TSC1 or TSC2 genes, resulting in hyperactivation of the mTOR signaling pathway, which regulates cell growth, proliferation, survival, and autophagy. TSC1 and TSC2 are classified as tumor suppressor genes and function according to Knudson’s two-hit hypothesis, which requires both alleles to be damaged for tumor formation. However, a second-hit mutation is a rare event in cortical tubers. This suggests that the molecular mechanism of cortical tuber formation may be more complicated and requires further research. This review highlights the issues of molecular genetics and genotype–phenotype correlations, considers histopathological characteristics and the mechanism of morphogenesis of cortical tubers, and also presents data on the relationship between these formations and the development of neurological manifestations, as well as treatment options. Full article

(This article belongs to the Special Issue Neuropathology: From Molecular Mechanisms to Therapeutic Solutions)

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