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Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition
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Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 5868

Special Issue Editors

Prof. Dr. Ramunė Morkūnienė

E-Mail Website
Guest Editor
1. Faculty of Pharmacy, Lithuanian University of Health Sciences, Kaunas, Lithuania
2. Neuroscience Institute, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: cell death; energy metabolism; mitochondria; inflammation; neurodegenerative disorders; ischemia/reperfusion; amyloid proteins; brain cell cultures
Special Issues, Collections and Topics in MDPI journals
Dr. Dalia M. Kopustinskiene

E-Mail Website
Guest Editor
Faculty of Pharmacy, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: protective and toxic mechanisms of bioactive compounds; ischemia; anoxia; stress conditions; cellular energy turnover; mitochondrial functions; ion channels; computer modeling in drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The world’s population is aging. Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, etc. In addition, aging is the strongest risk factor for ischemic stroke, and brain ischemia could progress and lead to the development of neurodegeneration. Both pathologies are life-threatening and may cause death or severe complications. Consequently, new therapies are constantly being sought out and one of the research directions is a search for effective neuroprotective agents. Oxidative stress, mitochondrial injury, and inflammation activation leading to brain cell death have been suggested as key mechanisms of irreversible damage in many neurological disorders. The accumulation of several oxidation products in neurons during aging and pathological conditions supports the idea that the presence of natural antioxidant biomolecules may be a beneficial alternative therapy for neurodegeneration and other related diseases. Consequently, mitochondria-targeted or inflammatory response-regulated bioactive compounds may be promising candidate therapeutics for the prevention of brain cell death. We would like to invite you to submit original research papers or review articles to this Special Issue on “Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease”, addressing any research topic highlighting the recent identification of synthetic as well as natural-based bioactive molecules that alleviate brain cell damage.

Prof. Dr. Ramunė Morkūnienė
Dr. Dalia M. Kopustinskiene
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.

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. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • brain
  • neuroprotection
  • neurodegenerative diseases
  • ischemia
  • mitochondria
  • oxidative stress
  • inflammation
  • bioactive compounds

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Related Special Issue

Published Papers (6 papers)

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Research

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19 pages, 5980 KiB  
Article
Neuroprotective Effect of Flavonoid Agathisflavone in the Ex Vivo Cerebellar Slice Neonatal Ischemia
by Rodrigo Barreto Carreira, Cleonice Creusa dos Santos, Juciele Valeria Ribeiro de Oliveira, Victor Diogenes Amaral da Silva, Jorge Maurício David, Arthur Morgan Butt and Silvia Lima Costa
Molecules 2024, 29(17), 4159; https://doi.org/10.3390/molecules29174159 - 2 Sep 2024
Viewed by 531
Abstract
Agathisflavone is a flavonoid that exhibits anti-inflammatory and anti-oxidative properties. Here, we investigated the neuroprotective effects of agathisflavone on central nervous system (CNS) neurons and glia in the cerebellar slice ex vivo model of neonatal ischemia. Cerebellar slices from neonatal mice, in which [...] Read more.
Agathisflavone is a flavonoid that exhibits anti-inflammatory and anti-oxidative properties. Here, we investigated the neuroprotective effects of agathisflavone on central nervous system (CNS) neurons and glia in the cerebellar slice ex vivo model of neonatal ischemia. Cerebellar slices from neonatal mice, in which glial fibrillary acidic protein (GFAP) and SOX10 drive expression of enhanced green fluorescent protein (EGFP), were used to identify astrocytes and oligodendrocytes, respectively. Agathisflavone (10 μM) was administered preventively for 60 min before inducing ischemia by oxygen and glucose deprivation (OGD) for 60 min and compared to controls maintained in normal oxygen and glucose (OGN). The density of SOX-10+ oligodendrocyte lineage cells and NG2 immunopositive oligodendrocyte progenitor cells (OPCs) were not altered in OGD, but it resulted in significant oligodendroglial cell atrophy marked by the retraction of their processes, and this was prevented by agathisflavone. OGD caused marked axonal demyelination, determined by myelin basic protein (MBP) and neurofilament (NF70) immunofluorescence, and this was blocked by agathisflavone preventative treatment. OGD also resulted in astrocyte reactivity, exhibited by increased GFAP-EGFP fluorescence and decreased expression of glutamate synthetase (GS), and this was prevented by agathisflavone pretreatment. In addition, agathisflavone protected Purkinje neurons from ischemic damage, assessed by calbindin (CB) immunofluorescence. The results demonstrate that agathisflavone protects neuronal and myelin integrity in ischemia, which is associated with the modulation of glial responses in the face of ischemic damage. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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18 pages, 5303 KiB  
Article
In Vitro and In Silico Anti-Glioblastoma Activity of Hydroalcoholic Extracts of Artemisia annua L. and Artemisia vulgaris L.
by Jurga Bernatoniene, Emilija Nemickaite, Daiva Majiene, Mindaugas Marksa and Dalia M. Kopustinskiene
Molecules 2024, 29(11), 2460; https://doi.org/10.3390/molecules29112460 - 23 May 2024
Cited by 1 | Viewed by 1174
Abstract
Glioblastoma, the most aggressive and challenging brain tumor, is a key focus in neuro-oncology due to its rapid growth and poor prognosis. The C6 glioma cell line is often used as a glioblastoma model due to its close simulation of human glioma characteristics, [...] Read more.
Glioblastoma, the most aggressive and challenging brain tumor, is a key focus in neuro-oncology due to its rapid growth and poor prognosis. The C6 glioma cell line is often used as a glioblastoma model due to its close simulation of human glioma characteristics, including rapid expansion and invasiveness. Alongside, herbal medicine, particularly Artemisia spp., is gaining attention for its anticancer potential, offering mechanisms like apoptosis induction, cell cycle arrest, and the inhibition of angiogenesis. In this study, we optimized extraction conditions of polyphenols from Artemisia annua L. and Artemisia vulgaris L. herbs and investigated their anticancer effects in silico and in vitro. Molecular docking of the main phenolic compounds of A. annua and A. vulgaris and potential target proteins, including programmed cell death (apoptosis) pathway proteins proapoptotic Bax (PDB ID 6EB6), anti-apoptotic Bcl-2 (PDB ID G5M), and the necroptosis pathway protein (PDB ID 7MON), mixed lineage kinase domain-like protein (MLKL), in complex with receptor-interacting serine/threonine-protein kinase 3 (RIPK3), revealed the high probability of their interactions, highlighting the possible influence of chlorogenic acid in modulating necroptosis processes. The cell viability of rat C6 glioma cell line was assessed using a nuclear fluorescent double-staining assay with Hoechst 33342 and propidium iodide. The extracts from A. annua and A. vulgaris have demonstrated anticancer activity in the glioblastoma model, with the synergistic effects of their combined compounds surpassing the efficacy of any single compound. Our results suggest the potential of these extracts as a basis for developing more effective glioblastoma treatments, emphasizing the importance of further research into their mechanisms of action and therapeutic applications. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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13 pages, 767 KiB  
Article
Inhibition of Enzymes Involved in Neurodegenerative Disorders and Aβ1–40 Aggregation by Citrus limon Peel Polyphenol Extract
by Rosaria Arcone, Antonio D’Errico, Rosarita Nasso, Rosario Rullo, Annarita Poli, Paola Di Donato and Mariorosario Masullo
Molecules 2023, 28(17), 6332; https://doi.org/10.3390/molecules28176332 - 30 Aug 2023
Cited by 4 | Viewed by 1589
Abstract
Alzheimer’s (AD) and Parkinson’s diseases (PD) are multifactorial neurogenerative disorders of the Central Nervous System causing severe cognitive and motor deficits in elderly people. Because treatment of AD and PD by synthetic drugs alleviates the symptoms often inducing side effects, many studies have [...] Read more.
Alzheimer’s (AD) and Parkinson’s diseases (PD) are multifactorial neurogenerative disorders of the Central Nervous System causing severe cognitive and motor deficits in elderly people. Because treatment of AD and PD by synthetic drugs alleviates the symptoms often inducing side effects, many studies have aimed to find neuroprotective properties of diet polyphenols, compounds known to act on different cell signaling pathways. In this article, we analyzed the effect of polyphenols obtained from the agro-food industry waste of Citrus limon peel (LPE) on key enzymes of cholinergic and aminergic neurotransmission, such as butyryl cholinesterase (BuChE) and monoamine oxidases (MAO)-A/B, on Aβ1–40 aggregation and on superoxide dismutase (SOD) 1/2 that affect oxidative stress. In our in vitro assays, LPE acts as an enzyme inhibitor on BuChE (IC50 ~ 73 µM), MAO-A/B (IC50 ~ 80 µM), SOD 1/2 (IC50 ~ 10–20 µM) and interferes with Aβ1–40 peptide aggregation (IC50 ~ 170 µM). These results demonstrate that LPE behaves as a multitargeting agent against key factors of AD and PD by inhibiting to various extents BuChE, MAOs, and SODs and reducing Aβ-fibril aggregation. Therefore, LPE is a promising candidate for the prevention and management of AD and PD symptoms in combination with pharmacological therapies. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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Review

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20 pages, 1935 KiB  
Review
p38α Mitogen-Activated Protein Kinase—An Emerging Drug Target for the Treatment of Alzheimer’s Disease
by Jan Detka, Natalia Płachtij, Martyna Strzelec, Aleksandra Manik and Kinga Sałat
Molecules 2024, 29(18), 4354; https://doi.org/10.3390/molecules29184354 - 13 Sep 2024
Viewed by 368
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder, characterized by the formation of amyloid β and tau protein aggregates in the brain, neuroinflammation, impaired cholinergic neurotransmission, and oxidative stress, resulting in the gradual loss of neurons and neuronal function, which leads to cognitive and [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disorder, characterized by the formation of amyloid β and tau protein aggregates in the brain, neuroinflammation, impaired cholinergic neurotransmission, and oxidative stress, resulting in the gradual loss of neurons and neuronal function, which leads to cognitive and memory deficits in AD patients. Chronic neuroinflammation plays a particularly important role in the progression of AD since the excessive release of proinflammatory cytokines from glial cells (microglia and astrocytes) induces neuronal damage, which subsequently causes microglial activation, thus facilitating further neurodegenerative changes. Mitogen-activated protein kinase (MAPK) p38α is one of the key enzymes involved in the control of innate immune response. The increased activation of the p38α MAPK pathway, observed in AD, has been for a long time associated not only with the maintenance of excessive inflammatory process but is also linked with pathophysiological hallmarks of this disease, and therefore is currently considered an attractive drug target for novel AD therapeutics. This review aims to summarize the current state of knowledge about the involvement of p38α MAPK in different aspects of AD pathophysiology and also provides insight into the possible therapeutic effects of novel p38α MAPK inhibitors, which are currently studied as potential drug candidates for AD treatment. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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26 pages, 1973 KiB  
Review
Latest Perspectives on Alzheimer’s Disease Treatment: The Role of Blood-Brain Barrier and Antioxidant-Based Drug Delivery Systems
by Bianca Sânziana Daraban, Andrei Sabin Popa and Miruna S. Stan
Molecules 2024, 29(17), 4056; https://doi.org/10.3390/molecules29174056 - 27 Aug 2024
Viewed by 830
Abstract
There has been a growing interest recently in exploring the role of the blood-brain barrier (BBB) in the treatment of Alzheimer’s disease (AD), a neurodegenerative disorder characterized by cognitive decline and memory loss that affects millions of people worldwide. Research has shown that [...] Read more.
There has been a growing interest recently in exploring the role of the blood-brain barrier (BBB) in the treatment of Alzheimer’s disease (AD), a neurodegenerative disorder characterized by cognitive decline and memory loss that affects millions of people worldwide. Research has shown that the BBB plays a crucial role in regulating the entry of therapeutics into the brain. Also, the potential benefits of using antioxidant molecules for drug delivery were highlighted in Alzheimer’s treatment to enhance the therapeutic efficacy and reduce oxidative stress in affected patients. Antioxidant-based nanomedicine shows promise for treating AD by effectively crossing the BBB and targeting neuroinflammation, potentially slowing disease progression and improving cognitive function. Therefore, new drug delivery systems are being developed to overcome the BBB and improve the delivery of therapeutics to the brain, ultimately improving treatment outcomes for AD patients. In this context, the present review provides an in-depth analysis of recent advancements in AD treatment strategies, such as silica nanoparticles loaded with curcumin, selenium nanoparticles loaded with resveratrol, and many others, focusing on the critical role of the BBB and the use of antioxidant-based drug delivery systems. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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14 pages, 1719 KiB  
Review
Caveolae with GLP-1 and NMDA Receptors as Crossfire Points for the Innovative Treatment of Cognitive Dysfunction Associated with Neurodegenerative Diseases
by Moeka Nakashima, Naoko Suga, Sayuri Yoshikawa and Satoru Matsuda
Molecules 2024, 29(16), 3922; https://doi.org/10.3390/molecules29163922 - 20 Aug 2024
Viewed by 849
Abstract
Some neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that encompasses memory loss and/or apathy. Alzheimer’s disease is the most typical type of such neurodegenerative diseases that are characterized by deficits of cognition and alterations of behavior. Despite the huge [...] Read more.
Some neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that encompasses memory loss and/or apathy. Alzheimer’s disease is the most typical type of such neurodegenerative diseases that are characterized by deficits of cognition and alterations of behavior. Despite the huge efforts against Alzheimer’s disease, there has yet been no successful treatment for this disease. Interestingly, several possible risk genes for cognitive dysfunction are frequently expressed within brain cells, which may also be linked to cholesterol metabolism, lipid transport, exosomes, and/or caveolae formation, suggesting that caveolae may be a therapeutic target for cognitive dysfunctions. Interestingly, the modulation of autophagy/mitophagy with the alteration of glucagon-like peptide-1 (GLP-1) and N-methyl-d-aspartate (NMDA) receptor signaling may offer a novel approach to preventing and alleviating cognitive dysfunction. A paradigm showing that both GLP-1 and NMDA receptors at caveolae sites may be promising and crucial targets for the treatment of cognitive dysfunctions has been presented here, which may also be able to modify the progression of Alzheimer’s disease. This research direction may create the potential to move clinical care toward disease-modifying treatment strategies with maximal benefits for patients without detrimental adverse events for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition)
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