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Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets

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: 31 July 2025 | Viewed by 7742

Special Issue Editors

Dr. Michela Pecoraro

E-Mail Website
Guest Editor
Department of Pharmacy, University of Salerno, Via G. Paolo II, 84084 Fisciano, SA, Italy
Interests: oxidative stress; neurodegenerative diseases; misfolding protein; corrector; inflammation; ER stress; calcium homeostasis; proteostasis
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Franceschelli

E-Mail Website
Guest Editor
Department of Pharmacy, Division Biomedicine “Arturo Leone”, University of Salerno, Fisciano, Italy
Interests: ystic fibrosis (CF); inflammation; oxidative stress; ER stress; protein misfolding; signal transduction; cell trafficking
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue provides an in-depth exploration of the cellular and molecular intricacies underlying neurodegenerative disorders, focusing on previously unidentified mechanisms and promising drug candidates. This Special Issue also includes a study of cancer pathways, specifically neuroblastoma, to broaden the understanding of misfolded proteins’ role in various neurodegenerative conditions. Our primary goal is to investigate molecules capable of addressing pathologies arising from protein aggregates, which trigger chronic reticular stress. Through this multidisciplinary approach, this Special Issue aims to unveil novel therapeutic avenues for treating neurodegenerative diseases and neuroblastoma, potentially bringing new hope to patients and clinicians.

Dr. Michela Pecoraro
Dr. Silvia Franceschelli
Guest Editors

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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

  • neurodegenerative disease
  • oxidative stress
  • ER stress
  • mitochondrial stress
  • corrector
  • misfolding protein
  • preoteostasis
  • neuroblastoma

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Published Papers (5 papers)

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Research

15 pages, 10998 KiB  
Article
Evaluation of the Anti-Alzheimer Activity of Lycium barbarum Polysaccharide in Aβ1–42-Induced Neurotoxicity in Rat Model
by Qingxin Lu, Yixin Meng, Haichi Feng, Xin Di and Xiaoli Guo
Curr. Issues Mol. Biol. 2025, 47(4), 226; https://doi.org/10.3390/cimb47040226 - 26 Mar 2025
Viewed by 345
Abstract
As a common neurodegenerative disorder, Alzheimer’s disease (AD) manifests as progressive memory loss, cognitive deficits, and dementia in older adults. As the basis of the traditional Chinese medicinal herb Goji berries, Lycium barbarum polysaccharide (LBP) has been proven to exhibit multiple pharmacological activities, [...] Read more.
As a common neurodegenerative disorder, Alzheimer’s disease (AD) manifests as progressive memory loss, cognitive deficits, and dementia in older adults. As the basis of the traditional Chinese medicinal herb Goji berries, Lycium barbarum polysaccharide (LBP) has been proven to exhibit multiple pharmacological activities, including antioxidant, neuroprotective, and anti-inflammatory effects. Evidence supports that LBP can enhance cognitive function and holds promise in counteracting AD. In order to determine the neuroprotective effects of LBP, this study was conducted on an AD rat model induced by intracerebroventricular injection of Aβ1–42 peptides. From 24 h after induction until the end of the behavioral experiment, rats were orally administered LBP (150 and 300 mg/kg) once a day. Neurobehavioral parameters were evaluated starting 1 week after administration. After behavioral tests, rats were euthanized, and the whole brain and cortex were isolated to detect the variations in histopathology and biochemical parameters. LBP significantly reversed cognitive impairments, assessed through the Y-maze, Passive Avoidance Test (PAT), and Morris water maze (MWM) test, respectively. Furthermore, LBP not only attenuated NFκB, TNF-α, IL-1β, IL-6, AChE, and oxidative/nitrosative stress levels but also increased IL-4, IL-10, and ACh levels and ChAT activity in the cortex. HE staining also exhibited the neuroprotection of LBP. Our study findings imply that LBP may improve cognitive function through multiple mechanisms and is a potential anti-AD compound. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets)
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10 pages, 477 KiB  
Article
Amyloid Beta as a Candidate Blood Biomarker of Early Cognitive Decline in the Elderly—A Preliminary Study
by Oliwia McFarlane, Mariusz Kozakiewicz, Kornelia Kędziora-Kornatowska, Anita Gałęska-Śliwka and Milena Wojciechowska
Curr. Issues Mol. Biol. 2025, 47(3), 203; https://doi.org/10.3390/cimb47030203 - 18 Mar 2025
Viewed by 381
Abstract
(1) Background/Objectives: The pathogenic process of Alzheimer’s disease (AD) is known to begin decades before its clinical onset. This period, although imperceptible to the patient, encompasses a gradual neuronal loss. The first symptoms of dementia, often classified as mild cognitive impairment (MCI), in [...] Read more.
(1) Background/Objectives: The pathogenic process of Alzheimer’s disease (AD) is known to begin decades before its clinical onset. This period, although imperceptible to the patient, encompasses a gradual neuronal loss. The first symptoms of dementia, often classified as mild cognitive impairment (MCI), in many cases converts into incipient AD, but can also remain stable or even reverse to cognitive norm. An easy and fast blood-based method of identifying patients at risk of conversion to AD would allow for the application of disease-altering therapies. This preliminary study focuses on the identification and assessment of the relationship between plasma amyloid beta (Aβ) and cognitive performance in older Polish adults with respect to its adequacy as a biomarker of an early cognitive deterioration. (2) Methods: The preliminary research sample consisted of 230 participants, 109 females and 121 males, aged 65 plus. The association between plasma Aβ concentrations with cognitive status, gender, and age were assessed. The analyses were conducted in three categories of cognitive performance: cognitive norm, mild cognitive impairment, and mild dementia, based on results of the Mini-Mental State Examination (MMSE) and functional tests. (3) Results: No significant differences in plasma Aβ levels for different cognitive statuses were identified. No significant differences were found in Aβ levels based on age or gender. (4) Conclusions: In order to thoroughly explore the power of research on plasma Aβ with respect to early cognitive deterioration, further prospective studies are required. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets)
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18 pages, 5915 KiB  
Article
In Silico Analysis of miRNA-Regulated Pathways in Spinocerebellar Ataxia Type 7
by Verónica Marusa Borgonio-Cuadra, Aranza Meza-Dorantes, Nonanzit Pérez-Hernández, José Manuel Rodríguez-Pérez and Jonathan J. Magaña
Curr. Issues Mol. Biol. 2025, 47(3), 170; https://doi.org/10.3390/cimb47030170 - 2 Mar 2025
Viewed by 707
Abstract
Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disease characterized by cerebellar ataxia and retinal degeneration, caused by an abnormal expansion of the CAG trinucleotide in the coding region of the ATXN7 gene. Currently, in silico analysis is used to explore mechanisms [...] Read more.
Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disease characterized by cerebellar ataxia and retinal degeneration, caused by an abnormal expansion of the CAG trinucleotide in the coding region of the ATXN7 gene. Currently, in silico analysis is used to explore mechanisms and biological processes through bioinformatics predictions in various neurodegenerative diseases. Therefore, the aim of this study was to identify candidate human gene targets of four miRNAs (hsa-miR-29a-3p, hsa-miR-132-3p, hsa-miR-25-3p, and hsa-miR-92a-3p) involved in pathways that could play an important role in SCA7 pathogenesis through comprehensive in silico analysis including the prediction of miRNA target genes, Gen Ontology enrichment, identification of core genes in KEGG pathways, transcription factors and validated miRNA target genes with the mouse SCA7 transcriptome data. Our results showed the participation of the following pathways: adherens junction, focal adhesion, neurotrophin signaling, endoplasmic reticulum processing, actin cytoskeleton regulation, RNA transport, and apoptosis and dopaminergic synapse. In conclusion, unlike previous studies, we highlight using a bioinformatics approach the core genes and transcription factors involved in the different biological pathways and which ones are targets for the four miRNAs, which, in addition to being associated with neurodegenerative diseases, are also de-regulated in the plasma of patients with SCA7. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets)
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20 pages, 10282 KiB  
Article
Molecular Integrative Study on Inhibitory Effects of Pentapeptides on Polymerization and Cell Toxicity of Amyloid-β Peptide (1–42)
by Lianmeng Ye, Nuela Manka’a Che Ajuyo, Zhongyun Wu, Nan Yuan, Zhengpan Xiao, Wenyu Gu, Jiazheng Zhao, Yechun Pei, Yi Min and Dayong Wang
Curr. Issues Mol. Biol. 2024, 46(9), 10160-10179; https://doi.org/10.3390/cimb46090606 - 14 Sep 2024
Viewed by 1365
Abstract
Alzheimer’s Disease (AD) is a multifaceted neurodegenerative disease predominantly defined by the extracellular accumulation of amyloid-β (Aβ) peptide. In light of this, in the past decade, several clinical approaches have been used aiming at developing peptides for therapeutic use in AD. The use [...] Read more.
Alzheimer’s Disease (AD) is a multifaceted neurodegenerative disease predominantly defined by the extracellular accumulation of amyloid-β (Aβ) peptide. In light of this, in the past decade, several clinical approaches have been used aiming at developing peptides for therapeutic use in AD. The use of cationic arginine-rich peptides (CARPs) in targeting protein aggregations has been on the rise. Also, the process of peptide development employing computational approaches has attracted a lot of attention recently. Using a structure database containing pentapeptides made from 20 L-α amino acids, we employed molecular docking to sort pentapeptides that can bind to Aβ42, then performed molecular dynamics (MD) analyses, including analysis of the binding stability, interaction energy, and binding free energy to screen ligands. Transmission electron microscopy (TEM), circular dichroism (CD), thioflavin T (ThT) fluorescence detection of Aβ42 polymerization, MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay, and the flow cytometry of reactive oxygen species (ROS) were carried out to evaluate the influence of pentapeptides on the aggregation and cell toxicity of Aβ42. Two pentapeptides (TRRRR and ARRGR) were found to have strong effects on inhibiting the aggregation of Aβ42 and reducing the toxicity of Aβ42 secreted by SH-SY5Y cells, including cell death, reactive oxygen species (ROS) production, and apoptosis. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets)
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11 pages, 2944 KiB  
Article
Effects of Mucuna pruriens (L.) DC. and Levodopa in Improving Parkinson’s Disease in Rotenone Intoxicated Mice
by Sheher Bano Zaigham and Dong-Guk Paeng
Curr. Issues Mol. Biol. 2024, 46(8), 9234-9244; https://doi.org/10.3390/cimb46080545 - 22 Aug 2024
Cited by 1 | Viewed by 4399
Abstract
Parkinson’s disease (PD) is the second leading neurodegenerative disease after Alzheimer’s disease. Mucuna pruriens (L.) DC. (MP) is a plant that contains Levodopa (L-DOPA) and has been known to improve the symptoms of PD. In this preliminary study, we investigated the anti-parkinsonian potential [...] Read more.
Parkinson’s disease (PD) is the second leading neurodegenerative disease after Alzheimer’s disease. Mucuna pruriens (L.) DC. (MP) is a plant that contains Levodopa (L-DOPA) and has been known to improve the symptoms of PD. In this preliminary study, we investigated the anti-parkinsonian potential of MP to compare the effects of L-DOPA. We first developed an in vivo model of the PD in C57BL/6 male mice using rotenone. A total of twelve mice were used for this experiment. Nine mice were injected with rotenone (28 mg/kg) daily for 28 days. The mice experiments were performed to validate the effectiveness of MP to treat PD. Synthetic L-DOPA in a ratio of 1:20 with MP was used as MP contains 5% L-DOPA by weight in it. MP and L-DOPA were injected for 19 days on a daily basis. Cognitive function was evaluated using beam balance and olfactory tests. Serum analysis was performed using serum enzyme-linked immunosorbent assay (ELISA) analysis test. IL-12, IL-6, and TGF-β 1 were evaluated to validate the PD inducement and treatment. The levels of IL-12, IL-6, and TGF-β1 (p < 0.0001) in the PD mice group were significantly higher than those in the control group. The PD mice also showed higher latencies in beam balance and olfactory tests (p < 0.0001) compared to the control group. Both MP and L-DOPA-treated groups showed alleviation in latencies in beam balance and olfactory tests and decreased neuroinflammation in ELISA analysis (p < 0.001). The results treated by MP and L-DOPA showed insignificant differences in their values (p > 0.05). This proved that the MP and L-DOPA had similar effects in improving the symptoms of PD when used in the ratio of 1:20. Furthermore, both MP and L-DOPA reduced the level of IL-6 and TGF-β1 in this study. It may be inferred that a reduction in the level of IL-6 and TGF-β1 eventually leads to a reduction in the Th17 cells. The pathogenic Th17 is thought to be present in virtually all chronic inflammatory disorders. This can be an interesting area of research in further understanding the immunological effect of MP in ameliorating PD symptoms. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology Insights into Neurodegenerative Diseases: From Pathogenesis to Therapeutic Targets)
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