Neuroinflammation and Neuroinflammation-Induced Symptoms

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 11965

Special Issue Editor

Laboratories of Neuroimmunology, Department of Symptom Research, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
Interests: chemotherapy-induced neuropathy; fumarates; nerve injury; neuropathic pain; neuroinflammation; chronic pain

Special Issue Information

Dear Colleagues,

The Special Issue will mainly focus on neuroinflammation and neuroinflammation-induced symptoms, including injury-related pain, psychological stress, and epilepsy.

Neuroinflammation plays an important role in the pathogenesis of several neurological diseases. It is induced by pathogens, toxins, traumata, and degeneration. Neuroinflammation may have positive effects, such as enabling the nervous system and promoting regeneration. However, it may also become dysfunctional and exacerbate the outcomes of related symptoms. Thus, a thorough understanding of its mechanisms and therapeutic strategies is critical for public health benefits.

We invite authors in this exciting field to submit original research and review manuscripts to discuss the mechanisms and treatments of neuroinflammation.

Dr. Jiahe Li
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.

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Keywords

  • neuroinflammation
  • chemotherapy-induced neuropathy
  • chemotherapy-induced cognitive impairments
  • chronic pain
  • fatigue
  • depression
  • nerve injury
  • neuropathic pain
  • neurodegenerative disease
  • oxidative stress

Published Papers (4 papers)

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Research

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14 pages, 2322 KiB  
Article
Oral Treatment with d-RD2RD2 Impedes Early Disease Mechanisms in SOD1*G93A Transgenic Mice but Does Not Prolong Survival
by Katharina Wintz, Julia Post, Karl-Josef Langen, Dieter Willbold, Antje Willuweit and Janine Kutzsche
Biomedicines 2023, 11(4), 995; https://doi.org/10.3390/biomedicines11040995 - 23 Mar 2023
Cited by 2 | Viewed by 1469
Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting upper and lower motor neurons, thus, progressing to complete muscle loss until the patient dies from respiratory arrest. The disease is not curable, and patients die approximately 2–5 years after diagnosis. Studying the underlying [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting upper and lower motor neurons, thus, progressing to complete muscle loss until the patient dies from respiratory arrest. The disease is not curable, and patients die approximately 2–5 years after diagnosis. Studying the underlying disease mechanisms to get access to new treatment options is, therefore, essential for patients’ benefit. However, so far, only three drugs that alleviate the symptoms have been approved by the U.S. Food and Drug Administration (FDA). A new drug candidate for the treatment of ALS is the all-d-enantiomeric peptide RD2RD2. In this study, we investigated the therapeutic effect of RD2RD2 in two setups. First, we analyzed disease progression and survival in 7 week-old B6.Cg-Tg(SOD1*G93A)1Gur/J mice. Second, we confirmed the result of the survival analysis in the B6SJL-Tg(SOD1*G93A)1Gur/J mouse line. Shortly before disease onset, the mice were treated daily with an oral dose of 50 mg/kg body weight. Treatment with RD2RD2 led to a delayed disease onset and reduced motor phenotype as shown using the SHIRPA test, the splay reflex test, and the pole test, but did not affect survival. In conclusion, RD2RD2 has the ability to delay the onset of symptoms. Full article
(This article belongs to the Special Issue Neuroinflammation and Neuroinflammation-Induced Symptoms)
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15 pages, 2834 KiB  
Article
Synergistic Antinociceptive Effects of Indomethacin–Pregabalin and Meloxicam–Pregabalin in Paclitaxel-Induced Neuropathic Pain
by Yurong Ma, Wenwen Liu, Lingzhi Liang, Jiaqi Ye, Chaonan Huang, Tao Zhuang and Guisen Zhang
Biomedicines 2022, 10(6), 1413; https://doi.org/10.3390/biomedicines10061413 - 15 Jun 2022
Cited by 7 | Viewed by 2734
Abstract
Neuropathic pain is often closely associated with nerve injury or inflammation, and the role of traditional nonsteroidal anti-inflammatory drugs as adjuvants for treating chemotherapy-induced peripheral neuropathic pain remains unclear. In this study, the potential synergistic antinociceptive effects of indomethacin–pregabalin and meloxicam–pregabalin were evaluated [...] Read more.
Neuropathic pain is often closely associated with nerve injury or inflammation, and the role of traditional nonsteroidal anti-inflammatory drugs as adjuvants for treating chemotherapy-induced peripheral neuropathic pain remains unclear. In this study, the potential synergistic antinociceptive effects of indomethacin–pregabalin and meloxicam–pregabalin were evaluated in paclitaxel-induced neuropathic pain and carrageenan-induced inflammatory pain in rodents. Although indomethacin and meloxicam alone only slightly relieved mechanical allodynia in the above two models, isobolographic analysis showed that the combination of indomethacin or meloxicam with pregabalin produced significant synergistic antinociceptive effects for paclitaxel-induced neuropathic pain (IN-PGB, experimental ED25 = [4.41 (3.13–5.82)] mg/kg, theoretical ED25 = [8.50 (6.62–10.32)] mg/kg; MEL-PGB, experimental ED25 = [3.96 (2.62–5.46)] mg/kg, theoretical ED25 = [7.52 (5.73–9.39)] mg/kg). In addition, MEL-PGB dosed via intraplantar injection into the left paw, intragastric injection, or intraperitoneal injection reversed paclitaxel-induced allodynia, indicating that they may act at multiple sites in the neuroaxis and periphery. However, indomethacin–pregabalin and meloxicam–pregabalin exerted antagonistic antiallodynic interactions in carrageenan-induced inflammatory pain in rats. Taken together, coadministration of indomethacin or meloxicam with pregabalin may possess potential therapeutic advantages for treating chemotherapy-induced neuropathic pain. Full article
(This article belongs to the Special Issue Neuroinflammation and Neuroinflammation-Induced Symptoms)
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20 pages, 9907 KiB  
Article
The Effect of Coenzyme Q10 on Liver Injury Induced by Valproic Acid and Its Antiepileptic Activity in Rats
by Fahad Alqarni, Hala S. Eweis, Ahmed Ali, Aziza Alrafiah, Mohammed Alsieni, Shahid Karim and Mosleh Ayed Alkathyri
Biomedicines 2022, 10(1), 168; https://doi.org/10.3390/biomedicines10010168 - 13 Jan 2022
Cited by 7 | Viewed by 2243
Abstract
Valproic acid (VPA) has toxic metabolites that can elevate oxidative stress markers, and the hepatotoxicity of VPA has been reported. Coenzyme Q10 (CoQ10) is one of the most widely used antioxidants. The effect of CoQ10 on epileptogenesis and VPA hepatotoxicity were examined. Rats [...] Read more.
Valproic acid (VPA) has toxic metabolites that can elevate oxidative stress markers, and the hepatotoxicity of VPA has been reported. Coenzyme Q10 (CoQ10) is one of the most widely used antioxidants. The effect of CoQ10 on epileptogenesis and VPA hepatotoxicity were examined. Rats were randomly divided into five groups: the control group received 0.5% methylcellulose by oral gavages daily and saline by intraperitoneal injection three times weekly. The PTZ group received 1% methylcellulose by gavages daily and 30 mg/kg PTZ by intraperitoneal injection three times weekly. The valproic acid group received 500 mg/kg valproic acid by gavage and 30 mg/kg PTZ, as above. The CoQ10 group received 200 mg/kg CoQ10 by gavages daily and 30 mg/kg PTZ, as above. The Valproic acid + CoQ10 group received valproic acid and CoQ10, as above. Results: CoQ10 exhibited anticonvulsant activity and potentiated the anticonvulsant effect of VPA. CoQ10 combined with VPA induced a more significant reduction in oxidative stress and improved the histopathological changes in the brain and liver compared to VPA treatment. In addition, CoQ10 reduced the level of toxic VPA metabolites. These findings suggest that the co-administration of CoQ10 with VPA in epilepsy might have therapeutic potential by increasing antiepileptic activity and reducing the hepatotoxicity of VPA. Full article
(This article belongs to the Special Issue Neuroinflammation and Neuroinflammation-Induced Symptoms)
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Review

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13 pages, 350 KiB  
Review
Peripheral Neuropathies Derived from COVID-19: New Perspectives for Treatment
by Alfredo Córdova-Martínez, Alberto Caballero-García, Daniel Pérez-Valdecantos, Enrique Roche and David César Noriega-González
Biomedicines 2022, 10(5), 1051; https://doi.org/10.3390/biomedicines10051051 - 2 May 2022
Cited by 6 | Viewed by 4733
Abstract
Peripheral neuropathies constitute a group of disorders affecting the peripheral nervous system. Neuropathies have multiple causes such as infections (i.e., COVID-19), diabetes, and nutritional (low vitamin levels), among others. Many micronutrients, such as vitamins (A, C, D, E, B6, B12, and folate), certain [...] Read more.
Peripheral neuropathies constitute a group of disorders affecting the peripheral nervous system. Neuropathies have multiple causes such as infections (i.e., COVID-19), diabetes, and nutritional (low vitamin levels), among others. Many micronutrients, such as vitamins (A, C, D, E, B6, B12, and folate), certain minerals (Fe, Mg, Zn, Se, and Cu), and ω-3 fatty acids have immunomodulatory effects. Therefore, they may play an instrumental role in the treatment of COVID-19 infection. However, many COVID-19 patients can undergo neuropathy. In this context, there is a wealth of information on a variety of first-, second-, and third-line treatment options. This review focuses on the application of nutraceutical strategies in order to improve the symptomatology of neuropathy and neuropathic pain in patients that suffered from COVID-19. Our aim is to provide an alternative vision to traditional medical-pharmacological treatment through nutraceuticals. Full article
(This article belongs to the Special Issue Neuroinflammation and Neuroinflammation-Induced Symptoms)
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