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Neuroprotective Strategies 2023
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Special Issue "Neuroprotective Strategies 2023"

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: 31 December 2023 | Viewed by 1612

Special Issue Editor

Prof. Dr. Katalin Prokai-Tatrai

E-Mail Website
Guest Editor
Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, USA
Interests: drug design of central nervous system agents; neuropeptides and peptidomimetics; prodrugs for CNS delivery; CNS-selective estrogen therapy; neuroprotection; proteomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We started the “Neuroprotective Strategies” collection jointly with Molecules in 2009. It was a great success; a large number of reviews and original research articles were published in the inaugural volume. Since then, the International Journal of Molecular Sciences has successfully continued this collection, covering neuroprotection broadly, including, but not limited to, preclinical/basic science assessments of various animal models relevant to diseases and agents with potential or perceived translation values. We open up the “Neuroprotective Strategies” Topical Collection to thought-provoking comments, opinions and perspectives, in addition to our traditional reviews and research articles in this field. We especially encourage submissions that address critical issues having prevented successful clinical translations of promising laboratory data. The limitations of in vitro studies and preclinical animal models to mirror multiple pathologies underlying human neurodegenerative diseases, lack of drug-likeness of experimental agents, the need to consider absorption, distribution, metabolism, elimination, toxicology (ADMET) and pharmacokinetics even in the early stage of drug discovery, and obstacles of drug delivery to the CNS are only some of the issues that come to mind regarding this matter. Critical reviews on relevant patent literature are also welcome. I give thanks for past contributions and look forward to receiving future contributions on the promising and challenging aspects of the field. The following links: https://www.mdpi.com/journal/ijms/special_issues/Neuroprotective_strategies_collection point to already published papers within this Special Issue.

Prof. Dr. Katalin Prokai-Tatrai
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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • age-related neurodegeneration

  • blood–brain barrier
  • CNS injury
  • cognition and dementia
  • drug delivery and drug-likeness
  • inflammation
  • in silico drug design and disease models
  • ischemia and reperfusion
  • oxidative stress
  • peripheral nervous system
  • stem cell
  • structure–activity relationship
  • translational medicine

Published Papers (2 papers)

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Research

15 pages, 2148 KiB  
Article
Differential Effects of Hypothermia and SZR72 on Cerebral Kynurenine and Kynurenic Acid in a Piglet Model of Hypoxic–Ischemic Encephalopathy
by
Ferenc Domoki
,
Valéria Tóth-Szűki
,
Viktória Kovács
,
Gábor Remzső
,
Tímea Körmöczi
,
László Vécsei
and
Róbert Berkecz
Int. J. Mol. Sci. 2023, 24(19), 14522; https://doi.org/10.3390/ijms241914522 - 25 Sep 2023
Viewed by 390
Abstract
Kynurenic acid (KYNA), an endogenous neuroprotectant with antiexcitotoxic, antioxidant, and anti-inflammatory effects, is synthesized through the tryptophan-kynurenine (KYN) pathway. We investigated whether brain KYN or KYNA levels were affected by asphyxia in a translational piglet model of hypoxic–ischemic encephalopathy (HIE). We also studied [...] Read more.
Kynurenic acid (KYNA), an endogenous neuroprotectant with antiexcitotoxic, antioxidant, and anti-inflammatory effects, is synthesized through the tryptophan-kynurenine (KYN) pathway. We investigated whether brain KYN or KYNA levels were affected by asphyxia in a translational piglet model of hypoxic–ischemic encephalopathy (HIE). We also studied brain levels of the putative blood–brain barrier (BBB) permeable neuroprotective KYNA analogue SZR72, and whether SZR72 or therapeutic hypothermia (TH) modified KYN or KYNA levels. KYN, KYNA, and SZR72 levels were determined using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry in five brain regions 24 h after 20 min of asphyxia in vehicle-, SZR72- and TH-treated newborn piglets (n = 6-6-6) and naive controls (n = 4). Endogenous brain KYN levels (median range 311.2–965.6 pmol/g) exceeded KYNA concentrations (4.5–6.0 pmol/g) ~100-fold. Asphyxia significantly increased cerebral KYN and KYNA levels in all regions (1512.0–3273.9 and 16.9–21.2 pmol/g, respectively), increasing the KYN/Tryptophan-, but retaining the KYNA/KYN ratio. SZR72 treatment resulted in very high cerebral SZR72 levels (13.2–33.2 nmol/g); however, KYN and KYNA levels remained similar to those of the vehicle-treated animals. However, TH virtually ameliorated asphyxia-induced elevations in brain KYN and KYNA levels. The present study reports for the first time that the KYN pathway is altered during HIE development in the piglet. SZR72 readily crosses the BBB in piglets but fails to affect cerebral KYNA levels. Beneficial effects of TH may include restoration of the tryptophan metabolism to pre-asphyxia levels. Full article
(This article belongs to the Special Issue Neuroprotective Strategies 2023)
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17 pages, 2446 KiB  
Article
Quetiapine Moderates Doxorubicin-Induced Cognitive Deficits: Influence of Oxidative Stress, Neuroinflammation, and Cellular Apoptosis
by
Vasudevan Mani
and
Bander Shehail Alshammeri
Int. J. Mol. Sci. 2023, 24(14), 11525; https://doi.org/10.3390/ijms241411525 - 16 Jul 2023
Viewed by 868
Abstract
Chemotherapy is considered a major choice in cancer treatment. Unfortunately, several cognitive deficiencies and psychiatric complications have been reported in patients with cancer during treatment and for the rest of their lives. Doxorubicin (DOX) plays an important role in chemotherapy regimens but affects [...] Read more.
Chemotherapy is considered a major choice in cancer treatment. Unfortunately, several cognitive deficiencies and psychiatric complications have been reported in patients with cancer during treatment and for the rest of their lives. Doxorubicin (DOX) plays an important role in chemotherapy regimens but affects both the central and peripheral nervous systems. Antipsychotic drugs alleviate the behavioral symptoms of aging-related dementia, and the atypical class, quetiapine (QUET), has been shown to have beneficial effects on various cognitive impairments. The present investigation aimed to determine the possible mechanism underlying the effect of thirty-day administrations of QUET (10 or 20 mg/kg, p.o.) on DOX-induced cognitive deficits (DICDs). DICDs were achieved through four doses of DOX (2 mg/kg, i.p.) at an interval of seven days during drug treatment. Elevated plus maze (EPM), novel object recognition (NOR), and Y-maze tasks were performed to confirm the DICDs and find the impact of QUET on them. The ELISA tests were executed with oxidative [malondialdehyde (MDA), catalase, and reduced glutathione (GSH)], inflammatory [cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB), and tumor necrosis factor-alpha (TNF-α)], and apoptosis [B-cell lymphoma 2 (Bcl2), Bcl2 associated X protein (Bax), and Caspase-3] markers were assessed in the brain homogenate to explore the related mechanisms. DICD lengthened the transfer latency time in EPM, shortened the exploration time of the novel object, reduced the discrimination ability of the objects in NOR, and lowered the number of arm entries and time spent in the novel arm. QUET alleviated DICD-related symptoms. In addition, QUET reduced neuronal oxidative stress by reducing MDA and elevating GSH levels in the rat brain. Moreover, it reduced neuronal inflammation by controlling the levels of COX-2, NF-κB, and TNF-α. By improving the Bcl-2 level and reducing both Bax and Caspase-3 levels, it protected against neuronal apoptosis. Collectively, our results supported that QUET may protect against DICD, which could be explained by the inhibition of neuronal inflammation and the attenuation of cellular apoptosis protecting against oxidative stress. Full article
(This article belongs to the Special Issue Neuroprotective Strategies 2023)
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