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Neuroinflammatory Mediator in Neurodegenerative Disease

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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: 20 July 2024 | Viewed by 6138

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Special Issue Editors

Dr. Laura Giannotti

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Guest Editor

Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy
Interests: blood platelets; third molar; Bio-Oss; thiamine; toxopyrimidine; enzymes

Prof. Dr. Luisa Siculella

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Guest Editor

Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy
Interests: effects of nutrients and hormones on the expression of genes involved in lipid metabolism

Special Issue Information

Dear Colleagues,

Neuroinflammation is one of the crucial mechanisms in the pathogenesis of various brain diseases. Understanding the processes underlying this phenomenon through screening analysis and implementation of next-generation therapies could help us to study and understand genomes and the relationship between genotype and phenotype.

The aim of this special issue is to report on recent advances in neurodegenerative pathologies studies. This includes, but is not limited to, the use of exome sequencing, RNA sequencing, gene expression profiling, specific gene functions, protein-protein interactions, epigenomics, genome-wide association studies, and genomic selection or prediction. In vitro, in vivo and clinical studies as well as bioinformatics tools and databases that facilitate the analysis of genomic data are also welcome.

We encourage you to contribute your studies and research to advance the understanding and control of these debilitating diseases. Sharing the results will enable significant advances in the field of neuroscience and further research to improve the quality of life for patients affected by neurodegenerative diseases.

Dr. Laura Giannotti
Prof. Dr. Luisa Siculella
Guest Editors

Manuscript Submission Information

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Keywords

neuroinflammation
pathogenesis
genotype
phenotype
neurodegenerative diseases
molecular mechanisms

Published Papers (5 papers)

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Research

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21 pages, 4391 KiB

Open AccessArticle

Factor H’s Control of Complement Activation Emerges as a Significant and Promising Therapeutic Target for Alzheimer’s Disease Treatment

by Iris Hasantari, Nabil Nicolas, Philippe Alzieu, Léa Leval, Andree Shalabi, Sylvain Grolleau and Virginie Dinet

Int. J. Mol. Sci. 2024, 25(4), 2272; https://doi.org/10.3390/ijms25042272 - 14 Feb 2024

Viewed by 784

Abstract

The complement is a component of the innate immune system designed to fight infections and tissue- or age-related damages. Complement activation creates an inflammatory microenvironment, which enhances cell death. Excessive complement inflammatory activity has been linked to alterations in the structure and functions of the blood–brain barrier, contributing to a poor prognosis for Alzheimer’s disease (AD). In the AD preclinical phase, individuals are often clinically asymptomatic despite evidence of AD neuropathology coupled with heightened inflammation. Considering the involvement of the complement system in the risk of developing AD, we hypothesize that inhibiting complement activation could reduce this inflammatory period observed even before clinical signs, thereby slowing down the onset/progression of AD. To validate our hypothesis, we injected complement inhibitor factor H into the brain of APP/PS1 AD mice at early or late stages of this pathology. Our results showed that the injection of factor H had effects on both the onset and progression of AD by reducing proinflammatory IL6, TNF-α, IL1β, MAC and amyloid beta levels. This reduction was associated with an increase in VGLUT1 and Psd95 synaptic transmission in the hippocampal region, leading to an improvement in cognitive functions. This study invites a reconsideration of factor H’s therapeutic potential for AD treatment. Full article

(This article belongs to the Special Issue Neuroinflammatory Mediator in Neurodegenerative Disease)

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11 pages, 1975 KiB

Open AccessArticle

An Emerging Strategy for Neuroinflammation Treatment: Combined Cannabidiol and Angiotensin Receptor Blockers Treatments Effectively Inhibit Glial Nitric Oxide Release

by Sigal Fleisher-Berkovich, Veronica Battaglia, Francesca Baratta, Paola Brusa, Yvonne Ventura, Nitzan Sharon, Arik Dahan, Massimo Collino and Shimon Ben-Shabat

Int. J. Mol. Sci. 2023, 24(22), 16254; https://doi.org/10.3390/ijms242216254 - 13 Nov 2023

Viewed by 1040

Abstract

Cannabidiol (CBD), the major non-psychoactive phytocannabinoid found in cannabis, has anti-neuroinflammatory properties. Despite the increasing use of CBD, little is known about its effect in combination with other substances. Combination therapy has been gaining attention recently, aiming to produce more efficient effects. Angiotensin II activates the angiotensin 1 receptor and regulates neuroinflammation and cognition. Angiotensin receptor 1 blockers (ARBs) were shown to be neuroprotective and prevent cognitive decline. The present study aimed to elucidate the combined role of CBD and ARBs in the modulation of lipopolysaccharide (LPS)-induced glial inflammation. While LPS significantly enhanced nitric oxide synthesis vs. the control, telmisartan and CBD, when administered alone, attenuated this effect by 60% and 36%, respectively. Exposure of LPS-stimulated cells to both compounds resulted in the 95% inhibition of glial nitric oxide release (additive effect). A synergistic inhibitory effect on nitric oxide release was observed when cells were co-treated with losartan (5 μM) and CBD (5 μM) (by 80%) compared to exposure to each compound alone (by 22% and 26%, respectively). Telmisartan and CBD given alone increased TNFα levels by 60% and 40%, respectively. CBD and telmisartan, when given together, attenuated the LPS-induced increase in TNFα levels without statistical significance. LPS-induced IL-17 release was attenuated by CBD with or without telmisartan (by 75%) or telmisartan alone (by 60%). LPS-induced Interferon-γ release was attenuated by 80% when telmisartan was administered in the absence or presence of CBD. Anti-inflammatory effects were recorded when CBD was combined with the known anti-inflammatory agent dimethyl fumarate (DMF)/monomethyl fumarate (MMF). A synergistic inhibitory effect of CBD and MMF on glial release of nitric oxide (by 77%) was observed compared to cells exposed to MMF (by 35%) or CBD (by 12%) alone. Overall, this study highlights the potential of new combinations of CBD (5 μM) with losartan (5 μM) or MMF (1 μM) to synergistically attenuate glial NO synthesis. Additive effects on NO production were observed when telmisartan (5 μM) and CBD (5 μM) were administered together to glial cells. Full article

(This article belongs to the Special Issue Neuroinflammatory Mediator in Neurodegenerative Disease)

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Review

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21 pages, 2002 KiB

Open AccessReview

Potential Therapeutic Targets to Modulate the Endocannabinoid System in Alzheimer’s Disease

by Hina Kanwal, Moris Sangineto, Martina Ciarnelli, Pasqualina Castaldo, Rosanna Villani, Antonino Davide Romano, Gaetano Serviddio and Tommaso Cassano

Int. J. Mol. Sci. 2024, 25(7), 4050; https://doi.org/10.3390/ijms25074050 - 05 Apr 2024

Viewed by 690

Abstract

Alzheimer’s disease (AD), the most common neurodegenerative disease (NDD), is characterized by chronic neuronal cell death through progressive loss of cognitive function. Amyloid beta (Aβ) deposition, neuroinflammation, oxidative stress, and hyperphosphorylated tau proteins are considered the hallmarks of AD pathology. Different therapeutic approaches approved by the Food and Drug Administration can only target a single altered pathway instead of various mechanisms that are involved in AD pathology, resulting in limited symptomatic relief and almost no effect in slowing down the disease progression. Growing evidence on modulating the components of the endocannabinoid system (ECS) proclaimed their neuroprotective effects by reducing neurochemical alterations and preventing cellular dysfunction. Recent studies on AD mouse models have reported that the inhibitors of the fatty acid amide hydrolase (FAAH) and monoacylglycerol (MAGL), hydrolytic enzymes for N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), respectively, might be promising candidates as therapeutical intervention. The FAAH and MAGL inhibitors alone or in combination seem to produce neuroprotection by reversing cognitive deficits along with Aβ-induced neuroinflammation, oxidative responses, and neuronal death, delaying AD progression. Their exact signaling mechanisms need to be elucidated for understanding the brain intrinsic repair mechanism. The aim of this review was to shed light on physiology and pathophysiology of AD and to summarize the experimental data on neuroprotective roles of FAAH and MAGL inhibitors. In this review, we have also included CB1R and CB2R modulators with their diverse roles to modulate ECS mediated responses such as anti-nociceptive, anxiolytic, and anti-inflammatory actions in AD. Future research would provide the directions in understanding the molecular mechanisms and development of new therapeutic interventions for the treatment of AD. Full article

(This article belongs to the Special Issue Neuroinflammatory Mediator in Neurodegenerative Disease)

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20 pages, 374 KiB

Open AccessReview

Personalized, Precision Medicine to Cure Alzheimer’s Dementia: Approach #1

by Jeffrey Fessel

Int. J. Mol. Sci. 2024, 25(7), 3909; https://doi.org/10.3390/ijms25073909 - 31 Mar 2024

Viewed by 692

Abstract

The goal of the treatment for Alzheimer’s dementia (AD) is the cure of dementia. A literature review revealed 18 major elements causing AD and 29 separate medications that address them. For any individual with AD, one is unlikely to discern which major causal elements produced dementia. Thus, for personalized, precision medicine, all causal elements must be treated so that each individual patient will have her or his causal elements addressed. Twenty-nine drugs cannot concomitantly be administered, so triple combinations of drugs taken from that list are suggested, and each triple combination can be administered sequentially, in any order. Ten combinations given over 13 weeks require 2.5 years, or if given over 26 weeks, they require 5.0 years. Such sequential treatment addresses all 18 elements and should cure dementia. In addition, any comorbid risk factors for AD whose first presence or worsening was within ±1 year of when AD first appeared should receive appropriate, standard treatment together with the sequential combinations. The article outlines a randomized clinical trial that is necessary to assess the safety and efficacy of the proposed treatments; it includes a triple-drug Rx for equipoise. Clinical trials should have durations of both 2.5 and 5.0 years unless the data safety monitoring board (DSMB) determines earlier success or futility since it is uncertain whether three or six months of treatment will be curative in humans, although studies in animals suggest that the briefer duration of treatment might be effective and restore defective neural tracts. Full article

(This article belongs to the Special Issue Neuroinflammatory Mediator in Neurodegenerative Disease)

19 pages, 681 KiB

Open AccessReview

Mast Cells in Autism Spectrum Disorder—The Enigma to Be Solved?

by Eleonora Kovacheva, Maria Gevezova, Michael Maes and Victoria Sarafian

Int. J. Mol. Sci. 2024, 25(5), 2651; https://doi.org/10.3390/ijms25052651 - 24 Feb 2024

Viewed by 2292

Abstract

Autism Spectrum Disorder (ASD) is a disturbance of neurodevelopment with a complicated pathogenesis and unidentified etiology. Many children with ASD have a history of “allergic symptoms”, often in the absence of mast cell (MC)-positive tests. Activation of MCs by various stimuli may release molecules related to inflammation and neurotoxicity, contributing to the development of ASD. The aim of the present paper is to enrich the current knowledge on the relationship between MCs and ASD by discussing key molecules and immune pathways associated with MCs in the pathogenesis of autism. Cytokines, essential marker molecules for MC degranulation and therapeutic targets, are also highlighted. Understanding the relationship between ASD and the activation of MCs, as well as the involved molecules and interactions, are the main points contributing to solving the enigma. Key molecules, associated with MCs, may provide new insights to the discovery of drug targets for modeling inflammation in ASD. Full article

(This article belongs to the Special Issue Neuroinflammatory Mediator in Neurodegenerative Disease)

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