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Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration
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Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration

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 (30 June 2023) | Viewed by 6883

Special Issue Editors

Dr. Alin Ciobica

E-Mail Website
Guest Editor
Department of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, B dul Carol I, No. 11, 700506 Iasi, Romania
Interests: neuropsychiatry; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Ioana-Miruna Balmus

E-Mail
Guest Editor
1. Department of Exact Sciences and Natural Sciences, Institute of Interdisciplinary Research, Alexandru Ioan Cuza University of Iasi, Alexandru Lapusneanu Street, No. 26, 700057 Iasi, Romania
2. CENEMED Platform for Interdisciplinary Research, Grigore T. Popa University of Medicine and Pharmacy, Universitatii Street, No. 16, 700115 Iasi, Romania
Interests: neuroscience; neurophysiology; neurology; neurodegeneration; gastroenterology; animal physiology; animal behaviour; biochemistry; enzymology; molecular biology; molecular genetics; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to our Special Issue in the International Journal of Molecular Sciences (IJMS), entitled “Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration”. This Issue will cover a selection of recent research topics and current review articles, reporting the latest updates on the molecular mechanisms underlying the pathophysiology of the neurological diseases in which neuronal loss and neurodegeneration are mainly seen.

The main pathological molecular mechanisms described in neurodegeneration revolve around the well-known amyloid cascade, neurofibrillary tangles, mitochondrial dysfunction, neuroinflammation, and oxidative stress theories. However, it was recently suggested that most of the neurodegenerative diseases are, in fact, complex impairments not necessarily limited to the central nervous system, but also manifesting multiple components and pathological perspectives. In this way, we encourage researchers to describe their new perspectives regarding the pathological mechanisms and their interactions in the manifestation of the mentioned diseases. Moreover, we would be happy to consider relevant reports regarding the less-studied or less-common neurodegenerative diseases, such as (but not limited to) motor neuron disease, sclerosis diseases, brain atrophy, and atypical dementias. 

The objective of this Special Issue is to bring additional evidence of the discrete interplay between neurodegeneration, neuroinflammation, and oxidative stress from various perspectives and to improve the understanding of the molecular mechanisms underlying common, yet untreatable neurodegenerative diseases and also rare neurodegenerative disorders whose pathomechanisms are scarcely described to date.

Dr. Alin Ciobica
Dr. Ioana-Miruna Balmus
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • aging
  • Alzheimer’s disease
  • dementia
  • motor neuron disease
  • neurodegeneration
  • neuroinflammation
  • oxidative stress
  • Parkinson’s disease
  • rare neurodegenerative diseases
  • traumatic brain injury

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Published Papers (3 papers)

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Research

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12 pages, 1518 KiB  
Article
Establishing Normal Serum Values of Neurofilament Light Chains and Glial Fibrillary Acidic Protein Considering the Effects of Age and Other Demographic Factors in Healthy Adults
by Alexander Rodero-Romero, Enric Monreal, Raquel Sainz-Amo, José Manuel García Domínguez, Noelia Villarrubia, Jose Luís Veiga-González, José Ignacio Fernández-Velasco, Haydee Goicochea-Briceño, Fernando Rodríguez-Jorge, Susana Sainz de la Maza, Juan Luís Chico-García, Alfonso Muriel, Jaime Masjuan, Lucienne Costa-Frossard and Luisa María Villar
Int. J. Mol. Sci. 2024, 25(14), 7808; https://doi.org/10.3390/ijms25147808 - 17 Jul 2024
Viewed by 941
Abstract
Multiple studies have shown the importance of blood-based biomarkers indicating axonal damage (serum neurofilament light chains [sNfL]) or astroglia activation (serum glial fibrillary acidic protein [sGFAP]) for monitoring different neurological diseases. However, normal values of these variables remain to be clearly defined, partly [...] Read more.
Multiple studies have shown the importance of blood-based biomarkers indicating axonal damage (serum neurofilament light chains [sNfL]) or astroglia activation (serum glial fibrillary acidic protein [sGFAP]) for monitoring different neurological diseases. However, normal values of these variables remain to be clearly defined, partly due to the influence of different demographic factors. We investigated demographic differences in a cohort of healthy volunteers. A cross-sectional study was conducted including 116 healthy controls with ages between 18 and 69 years (67.5% females; n = 79). sNfL and sGFAP concentrations were measured using single-molecule arrays. Age and body mass index affected sNfL values, and age was found to be the most important factor. The normal values changed with age, and we established normal values for individuals younger than 45 years as <10 pg/mL and for controls older than 45 years as <15 pg/mL. We established normal values at <10 pg/mL for individuals younger than 45 years and <15 pg/mL for older individuals. Alternatively, a Z-score of 1.5 was relevant for all controls. sGFAP was only affected by age. Differences in normal values were evident by 55 years. The highest normality limit for sGFAP was 140 pg/mL for controls under 55 years and 280 for older controls. We defined normal levels for sNfL and sGFAP and their corresponding age-associated changes. These data may contribute to the application of such variables in clinical practice. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration)
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Review

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28 pages, 2175 KiB  
Review
The Role of Potential Oxidative Biomarkers in the Prognosis of Acute Ischemic Stroke and the Exploration of Antioxidants as Possible Preventive and Treatment Options
by Fatima Zahra Kamal, Radu Lefter, Hassna Jaber, Ioana-Miruna Balmus, Alin Ciobica and Alin-Constantin Iordache
Int. J. Mol. Sci. 2023, 24(7), 6389; https://doi.org/10.3390/ijms24076389 - 28 Mar 2023
Cited by 14 | Viewed by 3366
Abstract
Ischemic strokes occur when the blood supply to a part of the brain is interrupted or reduced due to arterial blockage, and it often leads to damage to brain cells or death. According to a myriad of experimental studies, oxidative stress is an [...] Read more.
Ischemic strokes occur when the blood supply to a part of the brain is interrupted or reduced due to arterial blockage, and it often leads to damage to brain cells or death. According to a myriad of experimental studies, oxidative stress is an important pathophysiological mechanism of ischemic stroke. In this narrative review, we aimed to identify how the alterations of oxidative stress biomarkers could suggest a severity-reflecting diagnosis of ischemic stroke and how these interactions may provide new molecular targets for neuroprotective therapies. We performed an eligibility criteria-based search on three main scientific databases. We found that patients with acute ischemic stroke are characterized by increased oxidative stress markers levels, such as the total antioxidant capacity, F2-isoprostanes, hydroxynonenal, total and perchloric acid oxygen radical absorbance capacity (ORACTOT and ORACPCA), malondialdehyde (MDA), myeloperoxidase, and urinary 8-oxo-7,8-dihydro-2′-deoxyguanosine. Thus, acute ischemic stroke is causing significant oxidative stress and associated molecular and cellular damage. The assessment of these molecular markers could be useful in diagnosing ischemic stroke, finding its causes, predicting its severity and outcomes, reducing its impact on the cellular structures of the brain, and guiding preventive treatment towards antioxidant-based therapy as novel therapeutic alternatives. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration)
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Other

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12 pages, 2537 KiB  
Concept Paper
Analysis of Non-Amyloidogenic Mutations in APP Supports Loss of Function Hypothesis of Alzheimer’s Disease
by Meewhi Kim and Ilya Bezprozvanny
Int. J. Mol. Sci. 2023, 24(3), 2092; https://doi.org/10.3390/ijms24032092 - 20 Jan 2023
Cited by 4 | Viewed by 1947
Abstract
Proteolytic processing of amyloid precursor protein (APP) plays a critical role in pathogenesis of Azheimer’s disease (AD). Sequential cleavage of APP by β- and γ-secretases leads to generation of Aβ40 (non-amyloidogenic) and Aβ42 (amyloidogenic) peptides. Presenilin-1 (PS1) or presenilin-2 (PS2) act as catalytic [...] Read more.
Proteolytic processing of amyloid precursor protein (APP) plays a critical role in pathogenesis of Azheimer’s disease (AD). Sequential cleavage of APP by β- and γ-secretases leads to generation of Aβ40 (non-amyloidogenic) and Aβ42 (amyloidogenic) peptides. Presenilin-1 (PS1) or presenilin-2 (PS2) act as catalytic subunits of γ-secretase. Multiple familial AD (FAD) mutations in APP, PS1, or PS2 affect APP proteolysis by γ-secretase and influence levels of generated Aβ40 and Aβ42 peptides. The predominant idea in the field is the “amyloid hypothesis” that states that the resulting increase in Aβ42:Aβ40 ratio leads to “toxic gain of function” due to the accumulation of toxic Aβ42 plaques and oligomers. An alternative hypothesis based on analysis of PS1 conditional knockout mice is that “loss of function” of γ-secretase plays an important role in AD pathogenesis. In the present paper, we propose a mechanistic hypothesis that may potentially reconcile these divergent ideas and observations. We propose that the presence of soluble Aβ peptides in endosomal lumen (and secreted to the extracellular space) is essential for synaptic and neuronal function. Based on structural modeling of Aβ peptides, we concluded that Aβ42 peptides and Aβ40 peptides containing non-amyloidogenic FAD mutations in APP have increased the energy of association with the membranes, resulting in reduced levels of soluble Aβ in endosomal compartments. Analysis of PS1-FAD mutations also revealed that all of these mutations lead to significant reduction in both total levels of Aβ produced and in the Aβ40/Aβ42 ratio, suggesting that the concentration of soluble Aβ in the endosomal compartments is reduced as a result of these mutations. We further reasoned that similar changes in Aβ production may also occur as a result of age-related accumulation of cholesterol and lipid oxidation products in postsynaptic spines. Our analysis more easily reconciled with the “loss of γ-secretase function” hypothesis than with the “toxic gain of Aβ42 function” idea. These results may also explain why inhibitors of β- and γ- secretase failed in clinical trials, as these compounds are also expected to significantly reduce soluble Aβ levels in the endosomal compartments. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Brain Injury and Neurodegeneration)
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