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Biomedicines
Special Issues
The Molecular and Cellular Biology of Neuroprotection
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The Molecular and Cellular Biology of Neuroprotection

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 3760

Special Issue Editors

Dr. Elisa Martín-Montañez

E-Mail Website
Guest Editor
1. Department of Pharmacology, Faculty of Medicine, Campus Teatinos, University of Malaga, 29010 Malaga, Spain
2. Institute of Biomedical Research of Malaga (IBIMA), 29010 Malaga, Spain
Interests: oxidative stress; neuroprotection; memory enhancement; neurological disorders; pulmonary diseases; iron-deficiency; music therapy
Dr. Silvana Yanina Romero-Zerbo

E-Mail Website
Guest Editor
1. Department of Human Physiology, Faculty of Medicine, Campus Teatinos, University of Malaga, 29010 Malaga, Spain
2. Institute of Biomedical Research of Malaga (IBIMA), 29010 Malaga, Spain
Interests: oxidative stress; neuroprotection; neurological disorders; cannabinoid system; obesity; type 2 diabetes

Special Issue Information

Dear Colleagues,

Neurological disorders, including neurodegenerative diseases, neuropsychiatric disorders, dementia, seizures, strokes, brain tumors, and traumatic brain as well as spinal cord injuries, are a significant global health issue with complex etiologies and pathophysiology, in addition to poor therapeutic management. Neuroprotection describes strategies that protect, mitigate, or delay neuronal damage by intervening and inhibiting processes that cause neuronal dysfunction, or those that promote wound healing. Common mechanisms of neuronal injury include excitotoxicity, neuroinflammation, decreased delivery of oxygen and glucose, increased oxidative stress, mitochondrial dysfunction, cellular energy failure, iron accumulation, or protein misfolding and aggregation. A better understanding of these processes in terms of their molecular and cellular biology will promote translational research and therefore aid in the designing of new therapeutic strategies.

This Special Issue aims to present the most up-to-date findings regarding research targeting the mechanisms underlying different neurological disorders and neuroprotection strategies. It aims to provide a broad overview of novel advances in the field.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) studies at the molecular and cellular levels, pharmacology, functional foods and nutraceuticals, omics, and gene therapy as well as cell therapy approaches. We welcome the submission of preclinical in vitro and in vivo studies, as well as translational studies.

We look forward to receiving your contributions.

Dr. Elisa Martín-Montañez
Dr. Silvana Yanina Romero-Zerbo
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • neurological disorders
  • mechanism of neuronal injury
  • molecular biology
  • cellular biology
  • neuroprotection
  • pharmacotherapy
  • functional foods and nutraceuticals
  • advanced therapies

Published Papers (3 papers)

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Research

11 pages, 2708 KiB  
Article
Early Post-Natal Immune Activation Leads to Object Memory Deficits in Female Tsc2+/− Mice: The Importance of Including Both Sexes in Neuroscience Research
by Manuel F. López-Aranda, Karen Bach, Raymond Bui, Miranda Phan, Odilia Lu, Chirag Thadani, Alessandro Luchetti, Rochelle Mandanas, Isaiah Herrera, María Dolores López-Ávalos and Alcino J. Silva
Biomedicines 2024, 12(1), 203; https://doi.org/10.3390/biomedicines12010203 - 17 Jan 2024
Viewed by 983
Abstract
There is evidence that viral infections during pre-natal development constitute a risk factor for neuropsychiatric disorders and lead to learning and memory deficits. However, little is known about why viral infections during early post-natal development have a different impact on learning and memory [...] Read more.
There is evidence that viral infections during pre-natal development constitute a risk factor for neuropsychiatric disorders and lead to learning and memory deficits. However, little is known about why viral infections during early post-natal development have a different impact on learning and memory depending on the sex of the subject. We previously showed that early post-natal immune activation induces hippocampal-dependent social memory deficits in a male, but not in a female, mouse model of tuberous sclerosis complex (TSC; Tsc2+/− mice). Here, we explored the impact of a viral-like immune challenge in object memory. We demonstrate that early post-natal immune activation (during the first 2 weeks of life) leads to object memory deficits in female, but not male, mice that are heterozygous for a gene responsible for tuberous sclerosis complex (Tsc2+/− mice), while no effect was observed in wild type (WT) mice. Moreover, we found that the same immune activation in Tsc2+/− adult mice was not able to cause object memory deficits in females, which suggests that the early post-natal development stage constitutes a critical window for the effects of immune challenge on adult memory. Also, our results suggest that mTOR plays a critical role in the observed deficit in object memory in female Tsc2+/− mice. These results, together with previous results published by our laboratory, showing sex-specific memory deficits due to early post-natal immune activation, reinforce the necessity of using both males and females for research studies. This is especially true for studies related to immune activation, since the higher levels of estrogens in females are known to affect inflammation and to provide neuroprotection. Full article
(This article belongs to the Special Issue The Molecular and Cellular Biology of Neuroprotection)
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14 pages, 5246 KiB  
Article
Response Profiles of BV2 Microglia to IFN-γ and LPS Co-Stimulation and Priming
by Meng Liy Pan, Nur Nabilah Ahmad Puzi, Yin Yin Ooi, Rajesh Ramasamy and Sharmili Vidyadaran
Biomedicines 2023, 11(10), 2648; https://doi.org/10.3390/biomedicines11102648 - 27 Sep 2023
Cited by 1 | Viewed by 1392
Abstract
(1) Background: The latest research illustrates that microglia phenotype is not the binary ‘resting’ and ‘activated’ profiles. Instead, there is wide diversity in microglia states. Similarly, when testing different stimulation protocols for BV2 microglia, we discovered differences in the response of the cells [...] Read more.
(1) Background: The latest research illustrates that microglia phenotype is not the binary ‘resting’ and ‘activated’ profiles. Instead, there is wide diversity in microglia states. Similarly, when testing different stimulation protocols for BV2 microglia, we discovered differences in the response of the cells in terms of the production of intracellular ROS (iROS), nitric oxide (NO), CD40 expression, and migratory capacity. (2) Methods: BV2 microglia were treated with single interferon gamma (IFN-γ) stimulation, LPS/IFN-γ co-stimulation, and priming with IFN-γ followed by stimulation with LPS for 24 h. The responses of BV2 microglia were then assessed using the H2DCFDA test for iROS, the Griess assay for NO, immunophenotyping for CD40/CD11b/MHC II, and migration using a transwell apparatus. (3) Results: Single stimulation with IFN-γ induced NO but not ROS in BV2 microglia. Co-stimulation with LPS200IFN-γ2.5 induced a higher iROS production (a 9.2-fold increase) and CD40 expression (28031 ± 8810.2 MFI), compared to priming with primedIFN-γ50LPS100 (a 4.0-fold increase in ROS and 16764 ± 1210.8 MFI of CD40). Co-stimulation also induced cell migration. On the other hand, priming BV2 microglia (primedIFN-γ50LPS100) resulted in a higher NO production (64 ± 1.4 µM) compared to LPS200IFN-γ2.5 co-stimulation (44 ± 1.7 µM). Unexpectedly, priming inhibited BV2 migration. (4) Conclusions: Taken together, the findings from this project reveal the ability of co-stimulation and priming in stimulating microglia into an inflammatory phenotype, and the heterogeneity of microglia responses towards different stimulating approaches. Full article
(This article belongs to the Special Issue The Molecular and Cellular Biology of Neuroprotection)
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14 pages, 5203 KiB  
Article
Nicotinamide Deteriorates Post-Stroke Immunodepression Following Cerebral Ischemia–Reperfusion Injury in Mice
by Shih-Huang Tai, Liang-Chun Chao, Sheng-Yang Huang, Hsiao-Wen Lin, Ai-Hua Lee, Yi-Yun Chen and E-Jian Lee
Biomedicines 2023, 11(8), 2145; https://doi.org/10.3390/biomedicines11082145 - 30 Jul 2023
Cited by 4 | Viewed by 904
Abstract
(1) Background: Inducing experimental stroke leads to biphasic immune responses, where the early activation of immune functions is followed by severe immunosuppression accompanied by spleen and thymus atrophy. Nicotinamide, a water-soluble B-group vitamin, is a known neuroprotectant against brain ischemia in animal models. [...] Read more.
(1) Background: Inducing experimental stroke leads to biphasic immune responses, where the early activation of immune functions is followed by severe immunosuppression accompanied by spleen and thymus atrophy. Nicotinamide, a water-soluble B-group vitamin, is a known neuroprotectant against brain ischemia in animal models. We examined the effect of nicotinamide on the central and peripheral immune response in experimental stroke models. (2) Methods: Nicotinamide (500 mg/kg) or saline was intravenously administered to C57BL/6 mice during reperfusion after transiently occluding the middle cerebral artery or after LPS injection. On day 3, the animals were examined for behavioral performance and were then sacrificed to assess brain infarction, blood–brain barrier (BBB) integrity, and the composition of immune cells in the brain, thymus, spleen, and blood using flow cytometry. (3) Results: Nicotinamide reduced brain infarction and microglia/macrophage activation following MCAo (p < 0.05). Similarly, in LPS-injected mice, microglia/macrophage activation was decreased upon treatment with nicotinamide (p < 0.05), suggesting a direct inhibitory effect of nicotinamide on microglia/macrophage activation. Nicotinamide decreased the infiltration of neutrophils into the brain parenchyma and ameliorated Evans blue leakage (p < 0.05), suggesting that a decreased infiltration of neutrophils could, at least partially, be the result of a more integrated BBB structure following nicotinamide treatment. Our studies also revealed that administering nicotinamide led to retarded B-cell maturation in the spleen and subsequently decreased circulating B cells in the thymus and bloodstream (p < 0.05). (4) Conclusions: Cumulatively, nicotinamide decreased brain inflammation caused by ischemia–reperfusion injury, which was mediated by a direct anti-inflammatory effect of nicotinamide and an indirect protective effect on BBB integrity. Administering nicotinamide following brain ischemia resulted in a decrease in circulating B cells. This warrants attention with respect to future clinical applications. Full article
(This article belongs to the Special Issue The Molecular and Cellular Biology of Neuroprotection)
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