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Special Issue Editors

Dr. Lorenza Guarnieri

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Guest Editor

Section of Pharmacology, Science of Health Department, School of Medicine, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy
Interests: neurodegenerative disease; natural compounds; nutraceuticals; nutritional interventions; cognitive impairment

Dr. Francesca Bosco

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Guest Editor

Department of Health Sciences, Institute of Research for Food Safety and Health (IRC-FSH), University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy
Interests: neuroinflammation; neurodegeneration; nutraceuticals; cognitive impairment; natural compounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases result from a variety of pathological conditions characterized by significant cellular damage, abnormal protein presence and altered connections of the nervous system that can impair the patient's life quality. It is estimated that neurodegenerative diseases affect millions of individuals worldwide and the likelihood of developing neurodegenerative disease increases dramatically with age. The presence of abnormal proteins and increased oxidative stress contribute to accelerating neuroinflammatory and neurodegenerative processes. To date, considerable progress has been made in identifying the molecular mechanisms and pathways underlying neurodegenerative diseases; however, identifying safe and effective drug therapies for treating these disorders is very arduous. Pharmacological therapies in use for the treatment of neurodegenerative disease are still ineffective in modifying pathological changes and neurological disorders, and they provide only symptomatic relief; therefore, it is essential to seek new therapeutic strategies to treat these diseases. Natural compounds have aroused considerable interest in this field, also proving to be a possible alternative to the synthetic drugs used. Natural compounds may exert positive effects on aging-related changes in the brain and are capable of modulating neurological processes, given their ability to interact with neuronal–glial signaling pathways that are implicated in neuronal survival and function. In this Special Issue, we aim to bring together research from experts in the field highlighting the neuroprotective capabilities of natural compounds to identify future directions that will lead to discoveries and alternative therapies for neurological disorders.

Dr. Lorenza Guarnieri
Dr. Francesca Bosco
Guest Editors

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Keywords

neurodegenerative disease
neurodegeneration
neuroinflammation
nutritional interventions
brain damage
neurological diseases
natural compounds

Published Papers (2 papers)

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Research

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18 pages, 9544 KiB

Open AccessArticle

Rubia cordifolia L. Attenuates Diabetic Neuropathy by Inhibiting Apoptosis and Oxidative Stress in Rats

by Sweeti Bana, Nitin Kumar, Ali Sartaj, Abdulsalam Alhalmi, Ashraf Ahmed Qurtam, Fahd A. Nasr, Mohammed Al-Zharani, Neelam Singh, Praveen Gaur, Rosaline Mishra, Snigdha Bhardwaj, Hasan Ali and Radha Goel

Pharmaceuticals 2023, 16(11), 1586; https://0-doi-org.brum.beds.ac.uk/10.3390/ph16111586 - 09 Nov 2023

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Abstract

Background: Diabetic neuropathy is a debilitating manifestation of long-term diabetes mellitus. The present study explored the effects of the roots of Rubia cordifolia L. (R. cordifolia L.) in the Wistar rat model for diabetic neuropathy and possible neuroprotective, antidiabetic, and analgesic mechanisms underlying this effect. Materials and Methods: Rats were divided into five experimental groups. An amount of 0.25% carboxy methyl cellulose (CMC) in saline and streptozotocin (STZ) (60 mg/kg) was given to group 1 and group 2, respectively. Group 3 was treated with STZ and glibenclamide simultaneously while groups 4 and 5 were simultaneously treated with STZ and hydroalcoholic extract of the root of R. cordifolia, respectively. Hot plate and cold allodynias were used to evaluate the pain threshold. The antioxidant effects of R. cordifolia were assessed by measuring Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). At the end of the study, sciatic nerve and brain tissues were collected for histopathological study. Bcl-2 proteins, cleaved caspase-3, and Bax were assessed through the Western blot method. Results: R. cordifolia significantly attenuated paw withdrawal and tail flick latency in diabetic neuropathic rats. R. cordifolia significantly (p < 0.01) improved the levels of oxidative stress. It was found to decrease blood glucose levels and to increase animal weight in R. cordifolia-treated groups. Treatment with R. cordifolia suppressed the cleaved caspase-3 and reduced the Bax:Bcl2 ratio in sciatic nerve and brain tissue compared to the diabetic group. Histopathological analysis also revealed a marked improvement in architecture and loss of axons in brain and sciatic nerve tissues at a higher dose of R. cordifolia (400 mg/kg). Conclusion: R. cordifolia attenuated diabetic neuropathy through its antidiabetic and analgesic properties by ameliorating apoptosis and oxidative stress. Full article

(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects)

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Other

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9 pages, 791 KiB

Open AccessBrief Report

Using Nutraceuticals to Help Manage Traumatic Spinal Cord Injury

by Paul Stacey, Arun Mensinkai, Pankaj Bansal, Seyed-Hossein Hosseini, Andrew Lavigne, Basia Gwardjan, Sayna Leylachian, Zhihui (Joy) Deng, Vinjamuri Chari, Sandra Giles and Shanker Nesathurai

Pharmaceuticals 2024, 17(1), 71; https://0-doi-org.brum.beds.ac.uk/10.3390/ph17010071 - 04 Jan 2024

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Abstract

Traumatic spinal cord injury (TSCI) is a significant public health challenge that has an adverse impact on functional independence, quality of life, and life expectancy. Management of people’s chronic conditions is a key aspect of contemporary medical practice. Our study was an open label, single arm, prospective pilot study to evaluate the feasibility of treating people with TSCI. The study intervention was treatment with oral selenium and vitamin E. Participants were 18 years or older and experienced a TSCI at least one year prior to enrollment. Daily doses of 50 mcg of selenium and 400 IU of vitamin E were administered. Participants had radiologic (MRI tractography) and clinical (ASIA) assessments prior to initiating treatment, and these assessments were repeated after one year of treatment. Four subjects completed the full twelve-month study. Adherence, based on pill counts, was approximately 75% in all subjects. There were no adverse events related to study medications. During the treatment period, subjects reported improvement in certain symptoms. There was no significant difference in ASIA scores before and after the intervention. Combination treatment with vitamin E and selenium has been demonstrated as safe for TSCI patients. It is possible to use DTI values to locate the epicenter of a lesion as well as gauge the extent of injury. MRI tractography may serve as a meaningful surrogate endpoint. The results of this study suggest that it is feasible to conduct a larger long-term clinical trial to evaluate the efficacy of combination treatment of TSCI. Full article

(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects)

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