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Neuropharmacology and Neurodegenerative Diseases 2.0
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Neuropharmacology and Neurodegenerative Diseases 2.0

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: closed (30 August 2024) | Viewed by 3190

Special Issue Editor

Dr. Jessica Maiuolo

E-Mail Website
Guest Editor
IRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, Germaneto, 88100 Catanzaro, Italy
Interests: blood brain barrier; neurodegenerative diseases; cellular biology and pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are devastating conditions for which a cure has not yet been defined since the mechanisms involved are still little understood. The incidence of neurodegenerative conditions, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, among the others, has increased in recent decades, associated with an aging population and significant cost. Nowadays, increased inflammation and oxidative stress are considered key modulators and common denominators of these pathologies.

Neuropharmacology has been evolving rapidly in order to identify new strategies that can support the nervous system, reducing the load of these disorders. The few treatments that are known and used are hampered by the Blood–Brain Barrier (BBB), which does not allow for the translocation of many therapeutic agents from blood to the brain, thus preventing the development of specific and innovative therapies. Basic research on this topic moves in two important directions:

  • On the one hand, towards the synthesis of newly engineered materials, such as nanomaterials, and towards the development of nano- and biotechnology that can develop sophisticated drug delivery systems. In this case, in fact, nanodrugs, with particles smaller than 100 nm, could elude the BBB;
  • On the other hand, natural products or derivatives of plants, with known anti-inflammatory and antioxidant properties, could be tested.

Dr. Jessica Maiuolo
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.

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Keywords

  • neurodegenerative diseases
  • demyelinating diseases
  • blood–brain barrier
  • inflammation
  • reactive chemical species
  • mitochondria
  • endoplasmic reticulum
  • autophagy
  • apoptosis
  • nanodrugs
  • natural compounds
  • polyphenols

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Published Papers (2 papers)

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Research

18 pages, 6192 KiB  
Article
Sodium Tungstate Promotes Neurite Outgrowth and Confers Neuroprotection in Neuro2a and SH-SY5Y Cells
by Nora Montero-Martin, María D. Girón, José D. Vílchez and Rafael Salto
Int. J. Mol. Sci. 2024, 25(17), 9150; https://doi.org/10.3390/ijms25179150 - 23 Aug 2024
Viewed by 1003
Abstract
Sodium tungstate (Na2WO4) normalizes glucose metabolism in the liver and muscle, activating the Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. Because this pathway controls neuronal survival and differentiation, we investigated the effects of Na2WO4 in mouse [...] Read more.
Sodium tungstate (Na2WO4) normalizes glucose metabolism in the liver and muscle, activating the Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. Because this pathway controls neuronal survival and differentiation, we investigated the effects of Na2WO4 in mouse Neuro2a and human SH-SY5Y neuroblastoma monolayer cell cultures. Na2WO4 promotes differentiation to cholinergic neurites via an increased G1/G0 cell cycle in response to the synergic activation of the Phosphatidylinositol 3-kinase (PI3K/Akt) and ERK1/2 signaling pathways. In Neuro2a cells, Na2WO4 increases protein synthesis by activating the mechanistic target of rapamycin (mTOR) and S6K kinases and GLUT3-mediated glucose uptake, providing the energy and protein synthesis needed for neurite outgrowth. Furthermore, Na2WO4 increased the expression of myocyte enhancer factor 2D (MEF2D), a member of a family of transcription factors involved in neuronal survival and plasticity, through a post-translational mechanism that increases its half-life. Site-directed mutations of residues involved in the sumoylation of the protein abrogated the positive effects of Na2WO4 on the MEF2D-dependent transcriptional activity. In addition, the neuroprotective effects of Na2WO4 were evaluated in the presence of advanced glycation end products (AGEs). AGEs diminished neurite differentiation owing to a reduction in the G1/G0 cell cycle, concomitant with lower expression of MEF2D and the GLUT3 transporter. These negative effects were corrected in both cell lines after incubation with Na2WO4. These findings support the role of Na2WO4 in neuronal plasticity, albeit further experiments using 3D cultures, and animal models will be needed to validate the therapeutic potential of the compound. Full article
(This article belongs to the Special Issue Neuropharmacology and Neurodegenerative Diseases 2.0)
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17 pages, 2881 KiB  
Article
Hydroxytyrosol–Donepezil Hybrids Play a Protective Role in an In Vitro Induced Alzheimer’s Disease Model and in Neuronal Differentiated Human SH-SY5Y Neuroblastoma Cells
by Jessica Maiuolo, Paola Costanzo, Mariorosario Masullo, Antonio D’Errico, Rosarita Nasso, Sonia Bonacci, Vincenzo Mollace, Manuela Oliverio and Rosaria Arcone
Int. J. Mol. Sci. 2023, 24(17), 13461; https://doi.org/10.3390/ijms241713461 - 30 Aug 2023
Cited by 10 | Viewed by 1789
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative pathology among progressive dementias, and it is characterized by the accumulation in the brain of extracellular aggregates of beta-amyloid proteins and neurofibrillary intracellular tangles consisting of τ-hyperphosphorylated proteins. Under normal conditions, beta-amyloid peptides exert important [...] Read more.
Alzheimer’s disease (AD) is the most common neurodegenerative pathology among progressive dementias, and it is characterized by the accumulation in the brain of extracellular aggregates of beta-amyloid proteins and neurofibrillary intracellular tangles consisting of τ-hyperphosphorylated proteins. Under normal conditions, beta-amyloid peptides exert important trophic and antioxidant roles, while their massive presence leads to a cascade of events culminating in the onset of AD. The fibrils of beta-amyloid proteins are formed by the process of fibrillogenesis that, starting from individual monomers of beta-amyloid, can generate polymers of this protein, constituting the hypothesis of the “amyloid cascade”. To date, due to the lack of pharmacological treatment for AD without toxic side effects, chemical research is directed towards the realization of hybrid compounds that can act as an adjuvant in the treatment of this neurodegenerative pathology. The hybrid compounds used in this work include moieties of a hydroxytyrosol, a nitrohydroxytyrosol, a tyrosol, and a homovanillyl alcohol bound to the N-benzylpiperidine moiety of donepezil, the main drug used in AD. Previous experiments have shown different properties of these hybrids, including low toxicity and antioxidant and chelating activities. The purpose of this work was to test the effects of hybrid compounds mixed with Aβ 1–40 to induce fibrillogenesis and mimic AD pathogenesis. This condition has been studied both in test tubes and by an in vitro model of neuronal differentiated human SH-SY5Y neuroblastoma cells. The results obtained from test tube experiments showed that some hybrids inhibit the activity of the enzymes AChE, BuChE, and BACE-1. Cell experiments suggested that hybrids could inhibit fibrillogenesis, negatively modulating caspase-3. They were also shown to exert antioxidant effects, and the acetylated hybrids were found to be more functional and efficient than nonacetylated forms. Full article
(This article belongs to the Special Issue Neuropharmacology and Neurodegenerative Diseases 2.0)
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