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Cells
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Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives
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Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 9742

Special Issue Editors

Prof. Dr. Anthony Tsarbopoulos

E-Mail Website
Guest Editor
Department of Pharmacology, National and Kapodistrian, University of Athens, Athens, Greece
Interests: metabolic studies; protein–ligand interactions; protein aggregation processes in AD; metabolomics
Special Issues, Collections and Topics in MDPI journals
Dr. Nikolaos Kokras

E-Mail Website
Guest Editor
First Department of Psychiatry, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece
Interests: psychopharmacology; sex differences; antidepressants

Special Issue Information

Dear Colleagues,

The continuing demographic transition toward an aging society is leading to the growing prevalence of chronic age-related diseases. This is extremely important due to the lack of effective treatment and associated immense socioeconomic burden on all industrialized countries. Neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are persistent progressive diseases associated with an abnormal accumulation and aggregation of disease-specific proteins and peptides. Such changes have been linked to a noticeable activation of immune responses, increased levels of oxidative stress and neuronal cell death. Even though there has been tremendous knowledge growth into the disease mechanisms of neurodegenerative disorders, there is a great need for developing effective disease-modifying agents. Medicinal plants have been used for their “anti-aging” and cognitive enhancing properties. In view of a suggested mechanistic link between oxidative stress, inflammation and neurodegeneration, plant-derived neuroprotective compounds and dietary antioxidants may offer a promising therapeutic route for modifying the progression or protecting against the risk of neurodegenerative diseases.

Prof. Dr. Anthony Tsarbopoulos
Dr. Nikolaos Kokras
Guest Editors

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Keywords

  • bioactive compounds
  • protein aggregation processes in AD
  • cognitive, anxiolytic and antidepressant effects

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Published Papers (4 papers)

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Research

21 pages, 4834 KiB  
Article
Neuroprotective Effect of Mixed Mushroom Mycelia Extract on Neurotoxicity and Neuroinflammation via Regulation of ROS-Induced Oxidative Stress in PC12 and BV2 Cells
by Sang-Seop Lee, Da-Hyun Ko, Ga-Young Lee, So-Yeon Kim, Seung-Yun Han, Jong-Yea Park, MiNa Park, Hyun-Min Kim, Ya-El Kim and Yung-Choon Yoo
Cells 2025, 14(13), 977; https://doi.org/10.3390/cells14130977 (registering DOI) - 25 Jun 2025
Viewed by 128
Abstract
In this study, we investigated the potential of a three-mushroom complex extract (GMK) to inhibit neuronal cell death induced by the activation of AMPA and NMDA receptors following glutamate treatment in NGF-differentiated PC12 neuronal cells. GMK significantly mitigated glutamate-induced excitotoxic neuronal apoptosis by [...] Read more.
In this study, we investigated the potential of a three-mushroom complex extract (GMK) to inhibit neuronal cell death induced by the activation of AMPA and NMDA receptors following glutamate treatment in NGF-differentiated PC12 neuronal cells. GMK significantly mitigated glutamate-induced excitotoxic neuronal apoptosis by reducing the elevated expression of BAX, a critical regulator of apoptosis, and restoring BCL2 levels. These neuroprotective effects were associated with redox regulation, as evidenced by the upregulation of SOD, CAT, and GSH levels, and the downregulation of MDA levels. Mechanistic studies further revealed that GMK effectively scavenged ROS by downregulating NOX1, NOX2, and NOX4, while upregulating NRF1, P62, NRF2, HO1, and NQO1. Additionally, in the same model, GMK treatment increased acetylcholine, choline acetyltransferase, and GABA levels while reducing acetylcholinesterase activity. These effects were also attributed to the regulation of redox balance. Furthermore, we investigated the antioxidant and anti-inflammatory mechanisms of GMK in LPS-stimulated BV2 microglia. GMK inhibited the activation of IκB and MAPK pathways, positively regulated the BCL2/BAX ratio, suppressed TXNIP activity, and upregulated NQO1 and NOX1. In conclusion, GMK improved neuronal excitotoxicity and microglial inflammation through the positive modulation of the redox regulatory system, demonstrating its potential as a natural resource for pharmaceutical applications and functional health foods. Full article
(This article belongs to the Special Issue Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives)
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22 pages, 3926 KiB  
Article
Avenanthramide-C as Alzheimer’s Disease-Modifying Therapy: Early and Sustained Intervention Prevents Disease Progression in Mouse Models
by Alen Benhur Pravin Nathan, Areeba Aziz, Semyeong Choi, Seunghee Lee, Seyoung Jeon, Hyung-Seok Kim, Jonghyun Cho and Jihoon Jo
Cells 2025, 14(11), 826; https://doi.org/10.3390/cells14110826 - 2 Jun 2025
Viewed by 621
Abstract
Most approved drugs for Alzheimer’s disease (AD) are indicated for early to moderate stages and primarily target amyloid-beta or neurotransmitter systems. While these treatments may slow cognitive decline, they do not halt disease progression and are often limited by high cost and modest [...] Read more.
Most approved drugs for Alzheimer’s disease (AD) are indicated for early to moderate stages and primarily target amyloid-beta or neurotransmitter systems. While these treatments may slow cognitive decline, they do not halt disease progression and are often limited by high cost and modest efficacy. Natural compounds are increasingly being explored as alternative interventions. Our previous study showed that oral administration of Avenanthramide-C (Avn-C), a natural polyphenol from oats, for 14 days from early AD stages improved cognition and reduced neuroinflammation in AD mice. To assess its long-term potential, in this study we extended Avn-C treatment to three months starting from early disease stages in 5xFAD and Tg2576 models. Sustained administration preserved recovered long-term potentiation (LTP) by maintaining AMPK activation and inhibiting caspase-3 and GSK3β, thereby reducing amyloid accumulation and tau hyperphosphorylation in the hippocampus. Avn-C also maintained anti-inflammatory effects by suppressing NF-κB-mediated proinflammatory cytokine release and preventing chronic microglial activation. This promoted microglial coverage of plaques in vivo and enhanced phagocytosis in vitro. Our findings suggest that early and sustained Avn-C treatment preserves cognitive function, modulates multiple pathological pathways, and may slow or prevent AD progression by targeting early neurodegenerative processes before irreversible damage occurs. Full article
(This article belongs to the Special Issue Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives)
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22 pages, 3953 KiB  
Article
Flaxseed Oil Alleviates Trimethyltin-Induced Cell Injury and Inhibits the Pro-Inflammatory Activation of Astrocytes in the Hippocampus of Female Rats
by Nataša Mitrović, Marija Adžić Bukvić, Marina Zarić Kontić, Milorad Dragić, Snježana Petrović, Marija Paunović, Vesna Vučić and Ivana Grković
Cells 2024, 13(14), 1184; https://doi.org/10.3390/cells13141184 - 11 Jul 2024
Cited by 1 | Viewed by 1881
Abstract
Exposure to the neurotoxin trimethyltin (TMT) selectively induces hippocampal neuronal injury and astrocyte activation accompanied with resultant neuroinflammation, which causes severe behavioral, cognitive, and memory impairment. A large body of evidence suggests that flaxseed oil (FSO), as one of the richest sources of [...] Read more.
Exposure to the neurotoxin trimethyltin (TMT) selectively induces hippocampal neuronal injury and astrocyte activation accompanied with resultant neuroinflammation, which causes severe behavioral, cognitive, and memory impairment. A large body of evidence suggests that flaxseed oil (FSO), as one of the richest sources of essential omega-3 fatty acids, i.e., α-linolenic acids (ALA), displays neuroprotective properties. Here, we report the preventive effects of dietary FSO treatment in a rat model of TMT intoxication. The administration of FSO (1 mL/kg, orally) before and over the course of TMT intoxication (a single dose, 8 mg/kg, i.p.) reduced hippocampal cell death, prevented the activation of astrocytes, and inhibited their polarization toward a pro-inflammatory/neurotoxic phenotype. The underlying protective mechanism was delineated through the selective upregulation of BDNF and PI3K/Akt and the suppression of ERK activation in the hippocampus. Pretreatment with FSO reduced cell death and efficiently suppressed the expression of inflammatory molecules. These beneficial effects were accompanied by an increased intrahippocampal content of n-3 fatty acids. In vitro, ALA pretreatment prevented the TMT-induced polarization of cultured astrocytes towards the pro-inflammatory spectrum. Together, these findings support the beneficial neuroprotective properties of FSO/ALA against TMT-induced neurodegeneration and accompanied inflammation and hint at a promising preventive use of FSO in hippocampal degeneration and dysfunction. Full article
(This article belongs to the Special Issue Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives)
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12 pages, 2199 KiB  
Communication
Ergothioneine Prevents Neuronal Cell Death Caused by the Neurotoxin 6-Hydroxydopamine
by Saho Yuzawa, Motonari Nakashio, Suzuna Ichimura, Mikako Shimoda, Ayaka Nakashima, Yuka Marukawa-Hashimoto, Yusuke Kawano, Kengo Suzuki, Kenichi Yoshitomi, Masahiro Kawahara and Ken-ichiro Tanaka
Cells 2024, 13(3), 230; https://doi.org/10.3390/cells13030230 - 25 Jan 2024
Cited by 6 | Viewed by 5885
Abstract
Neuronal cell death is a key mechanism involved in the development and exacerbation of Parkinson’s disease (PD). The excessive production of reactive oxygen species (ROS) is a major cause leading to neuronal death; therefore, compounds that prevent oxidative stress-dependent neuronal death may be [...] Read more.
Neuronal cell death is a key mechanism involved in the development and exacerbation of Parkinson’s disease (PD). The excessive production of reactive oxygen species (ROS) is a major cause leading to neuronal death; therefore, compounds that prevent oxidative stress-dependent neuronal death may be promising as a preventive method for PD. Ergothioneine is a natural amino acid with antioxidant properties, and its protective functions in the body are attracting attention. However, there has been no investigation into the protective functions of ergothioneine using in vivo and in vitro PD models. Thus, in this study, we analyzed the efficacy of ergothioneine against 6-hydroxydopamine (6-OHDA)-dependent neuronal cell death using immortalized hypothalamic neurons (GT1-7 cells). First, we found that ergothioneine prevents 6-OHDA-dependent neuronal cell death by suppressing ROS overproduction in GT1-7 cells. The cytoprotective effect of ergothioneine was partially abolished by verapamil, an inhibitor of OCTN1, which is involved in ergothioneine uptake. Furthermore, ergothioneine-rich Rice-koji (Ergo-koji) showed cytoprotective and antioxidant effects similar to those of ergothioneine. Taken together, these results suggest that ergothioneine or foods containing ergothioneine may be an effective method for preventing the development and progression of PD. Full article
(This article belongs to the Special Issue Natural Products in Neurodegenerative Diseases: Current Trends and Future Perspectives)
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