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Plasticity in Neurodegenerative Diseases

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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: closed (31 May 2023) | Viewed by 11115

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Prof. Dr. Rosario Gulino

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Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 97, 95123 Catania, Italy
Interests: spinal cord; motoneurons; cell death; neurotoxin; motoneuron disease; synaptic plasticity; animal model

Special Issue Information

Dear Colleagues,

Plastic changes, such as synaptic plasticity, synaptogenesis, fiber sprouting, dendritic remodeling and metabolic changes are typical events in learning and memory, but they are also present in different events of activity-dependent modification of neural circuits, including those responsible for compensatory changes occurring after different injury events, including stroke or mechanical damage of the central nervous system.

It is known that alterations of synapses are among the pathogenic mechanisms of different neurodegenerative diseases but, interestingly, an increasing body of evidence suggests that neuroplasticity could be responsible for compensatory attempts during disease progression. As a result, symptom onset usually occurs long after the initiation of neuronal degeneration. Although these compensatory plastic changes are unable to halt disease progression, they represent an important mechanism to be further studied, as well as a promising target for combined therapy approaches.

The aim of this special issue is to collect studies focused on different neurodegenerative diseases, including but not limited to the main ones, which share a common interest to the role of plasticity in the different phases of pathogenesis. Original articles and reviews are welcome.

Prof. Dr. Rosario Gulino
Guest Editor

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Keywords

synaptic plasticity
degeneration and regeneration
neurodegenerative disease
dendritic remodeling
axonal sprouting
metabolic changes
compensatory changes
neuroprotection

Published Papers (5 papers)

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Research

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15 pages, 308 KiB

Open AccessArticle

The Influence of Copper Nanoparticles on Neurometabolism Marker Levels in the Brain and Intestine in a Rat Model

by Monika Cendrowska-Pinkosz, Magdalena Krauze, Jerzy Juśkiewicz, Bartosz Fotschki and Katarzyna Ognik

Int. J. Mol. Sci. 2023, 24(14), 11321; https://doi.org/10.3390/ijms241411321 - 11 Jul 2023

Cited by 1 | Viewed by 1087

Abstract

The aim of this study is to assess the effect of different forms and dosages of copper on the levels of markers depicting the neurodegenerative changes in the brain and the jejunum. The experiment was performed using 40 male Wistar rats fed a typical rat diet with two dosages of Cu used as CuCO₃ (6.5 and 13 mg/kg diet) and dietary addition of two CuNP dosages (standard 6.5 and enhanced 13 mg/kg diet), randomly divided into four groups. The levels of neurodegenerative markers were evaluated. Nanoparticles caused a reduction in the level of glycosylated acetylcholinesterase (GAChE), an increase the level of acetylcholinesterase (AChE) and lipoprotein receptor-related protein 1 (LRP1), a reduction in β-amyloid (βAP) in the brain and in the intestine of rats and a reduction in Tau protein in the brain of rats. The highest levels of AChE, the ATP-binding cassette transporters (ABC) and LRP1 and lower levels of toxic GAChE, β-amyloid, Tau, hyper-phosphorylated Tau protein (p-Tau) and the complex of calmodulin and Ca²⁺ (CAMK2a) were recorded in the tissues of rats receiving a standard dose of Cu. The neuroprotective effect of Cu can be increased by replacing the carbonate form with nanoparticles and there is no need to increase the dose of copper. Full article

(This article belongs to the Special Issue Plasticity in Neurodegenerative Diseases)

16 pages, 1818 KiB

Open AccessArticle

A Meta-Analysis Study of SOD1-Mutant Mouse Models of ALS to Analyse the Determinants of Disease Onset and Progression

by Maria Ciuro, Maria Sangiorgio, Giampiero Leanza and Rosario Gulino

Int. J. Mol. Sci. 2023, 24(1), 216; https://doi.org/10.3390/ijms24010216 - 22 Dec 2022

Cited by 1 | Viewed by 2339

Abstract

A complex interaction between genetic and external factors determines the development of amyotrophic lateral sclerosis (ALS). Epidemiological studies on large patient cohorts have suggested that ALS is a multi-step disease, as symptom onset occurs only after exposure to a sequence of risk factors. Although the exact nature of these determinants remains to be clarified, it seems clear that: (i) genetic mutations may be responsible for one or more of these steps; (ii) other risk factors are probably linked to environment and/or to lifestyle, and (iii) compensatory plastic changes taking place during the ALS etiopathogenesis probably affect the timing of onset and progression of disease. Current knowledge on ALS mechanisms and therapeutic targets, derives mainly from studies involving superoxide dismutase 1 (SOD1) transgenic mice; therefore, it would be fundamental to verify whether a multi-step disease concept can also be applied to these animal models. With this aim, a meta-analysis study has been performed using a collection of primary studies (n = 137), selected according to the following criteria: (1) the studies should employ SOD1 transgenic mice; (2) the studies should entail the presence of a disease-modifying experimental manipulation; (3) the studies should make use of Kaplan–Meier plots showing the distribution of symptom onset and lifespan. Then, using a subset of this study collection (n = 94), the effects of treatments on key molecular mechanisms, as well as on the onset and progression of disease have been analysed in a large population of mice. The results are consistent with a multi-step etiopathogenesis of disease in ALS mice (including two to six steps, depending on the particular SOD1 mutation), closely resembling that observed in patient cohorts, and revealed an interesting relationship between molecular mechanisms and disease manifestation. Thus, SOD1 mouse models may be considered of high predictive value to understand the determinants of disease onset and progression, as well as to identify targets for therapeutic interventions. Full article

(This article belongs to the Special Issue Plasticity in Neurodegenerative Diseases)

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Review

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18 pages, 1593 KiB

Open AccessReview

Chitinase Signature in the Plasticity of Neurodegenerative Diseases

by Cristina Russo, Maria Stella Valle, Antonino Casabona and Lucia Malaguarnera

Int. J. Mol. Sci. 2023, 24(7), 6301; https://doi.org/10.3390/ijms24076301 - 27 Mar 2023

Cited by 3 | Viewed by 2024

Abstract

Several reports have pointed out that Chitinases are expressed and secreted by various cell types of central nervous system (CNS), including activated microglia and astrocytes. These cells play a key role in neuroinflammation and in the pathogenesis of many neurodegenerative disorders. Increased levels of Chitinases, in particular Chitotriosidase (CHIT-1) and chitinase-3-like protein 1 (CHI3L1), have been found increased in several neurodegenerative disorders. Although having important biological roles in inflammation, to date, the molecular mechanisms of Chitinase involvement in the pathogenesis of neurodegenerative disorders is not well-elucidated. Several studies showed that some Chitinases could be assumed as markers for diagnosis, prognosis, activity, and severity of a disease and therefore can be helpful in the choice of treatment. However, some studies showed controversial results. This review will discuss the potential of Chitinases in the pathogenesis of some neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, to understand their role as distinctive biomarkers of neuronal cell activity during neuroinflammatory processes. Knowledge of the role of Chitinases in neuronal cell activation could allow for the development of new methodologies for downregulating neuroinflammation and consequently for diminishing negative neurological disease outcomes. Full article

(This article belongs to the Special Issue Plasticity in Neurodegenerative Diseases)

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17 pages, 353 KiB

Open AccessReview

Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis

by Rosario Gulino

Int. J. Mol. Sci. 2023, 24(5), 4613; https://doi.org/10.3390/ijms24054613 - 27 Feb 2023

Cited by 9 | Viewed by 1568

Abstract

Recent evidence has supported the hypothesis that amyotrophic lateral sclerosis (ALS) is a multi-step disease, as the onset of symptoms occurs after sequential exposure to a defined number of risk factors. Despite the lack of precise identification of these disease determinants, it is known that genetic mutations may contribute to one or more of the steps leading to ALS onset, the remaining being linked to environmental factors and lifestyle. It also appears evident that compensatory plastic changes taking place at all levels of the nervous system during ALS etiopathogenesis may likely counteract the functional effects of neurodegeneration and affect the timing of disease onset and progression. Functional and structural events of synaptic plasticity probably represent the main mechanisms underlying this adaptive capability, causing a significant, although partial and transient, resiliency of the nervous system affected by a neurodegenerative disease. On the other hand, the failure of synaptic functions and plasticity may be part of the pathological process. The aim of this review was to summarize what it is known today about the controversial involvement of synapses in ALS etiopathogenesis, and an analysis of the literature, although not exhaustive, confirmed that synaptic dysfunction is an early pathogenetic process in ALS. Moreover, it appears that adequate modulation of structural and functional synaptic plasticity may likely support function sparing and delay disease progression. Full article

(This article belongs to the Special Issue Plasticity in Neurodegenerative Diseases)

20 pages, 1772 KiB

Open AccessReview

The Interplay between Ghrelin and Microglia in Neuroinflammation: Implications for Obesity and Neurodegenerative Diseases

by Cristina Russo, Maria Stella Valle, Antonella Russo and Lucia Malaguarnera

Int. J. Mol. Sci. 2022, 23(21), 13432; https://doi.org/10.3390/ijms232113432 - 03 Nov 2022

Cited by 11 | Viewed by 3418

Abstract

Numerous studies have shown that microglia are capable of producing a wide range of chemokines to promote inflammatory processes within the central nervous system (CNS). These cells share many phenotypical and functional characteristics with macrophages, suggesting that microglia participate in innate immune responses in the brain. Neuroinflammation induces neurometabolic alterations and increases in energy consumption. Microglia may constitute an important therapeutic target in neuroinflammation. Recent research has attempted to clarify the role of Ghre signaling in microglia on the regulation of energy balance, obesity, neuroinflammation and the occurrence of neurodegenerative diseases. These studies strongly suggest that Ghre modulates microglia activity and thus affects the pathophysiology of neurodegenerative diseases. This review aims to summarize what is known from the current literature on the way in which Ghre modulates microglial activity during neuroinflammation and their impact on neurometabolic alterations in neurodegenerative diseases. Understanding the role of Ghre in microglial activation/inhibition regulation could provide promising strategies for downregulating neuroinflammation and consequently for diminishing negative neurological outcomes. Full article

(This article belongs to the Special Issue Plasticity in Neurodegenerative Diseases)

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