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Ischemic Genetic Pathology 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 (15 April 2024) | Viewed by 3691

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Special Issue Editor

Prof. Dr. Ryszard Pluta

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Guest Editor

Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: brain ischemia versus Alzheimer's disease; brain ischemia; amyloid; tau protein; presenilins; α- and β-secretase; autophagy; mitophagy; apoptosis; apolipoproteins E, A1 and J; LRP1; RAGE; genes; neurodegeneration; dementia; Alzheimer's disease models
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Special Issue Information

Dear Colleagues,

The proper functioning of the brain depends to a large extent on the supply of oxygen and nutrients. Their deficiency or lack, e.g., due to focal or global cerebral ischemia, can lead to the death of neuronal cells and neurodegeneration. Cerebral ischemia significantly affects various cellular functions, starting from the immediate response to the lipid composition of the cell membrane, changes in enzyme activity, and mitochondrial remodeling, which in turn results in proteomic and genomic changes. Similar effects are caused by perinatal asphyxia, which has a significant impact on brain development and function, increasing the risk of developing various neurological pathologies later in life. The worst consequence of perinatal asphyxia is the aforementioned neurodegenerative brain injury with various cognitive impairments, also known as hypoxic-ischemic encephalopathy. There is increasing evidence that the pathology induced in neonatal brains during and after perinatal hypoxia and in adult ischemic stroke is almost identical to the pathology occurring in neurodegenerative diseases such as Alzheimer's disease. Brain ischemia and Alzheimer's disease share several common vascular risk factors. The pathophysiology of these diseases and whether one precedes the other is a topic of ongoing research. In this Special Issue, we would like to learn about each common pathway and the mechanisms of both neurodegenerative diseases. We would like to draw attention to the basic mechanisms of neurodegeneration and secondary cascades. Furthermore, the concept of early targeting of secondary mechanisms may be a viable treatment option. This Special Issue is intended to serve as a catalyst for further research into this important topic. Thanks to the involvement of scientists in this Special Issue, new different mechanisms/hypotheses of neurodegenerative diseases can be presented and discussed. This will allow us to better understand in the future which therapies may be most effective at specific points, such as on the Alzheimer's disease continuum. It is my hope that each article on this topic will both inform and generate further interest in the mechanisms explaining the development of dementia post-asphyxia, after ischemic stroke and Alzheimer's disease.

Prof. Dr. Ryszard Pluta
Guest Editor

Manuscript Submission Information

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Keywords

ischemic neurodegeneration
focal ischemia
global ischemia
perinatal asphyxia
stroke
Alzheimer’s disease
brain injury
genes involved in neurodegeneration
dementia
apnea

Published Papers (2 papers)

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Research

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11 pages, 1294 KiB

Open AccessArticle

Preservation of Biomarkers Associated with Alzheimer’s Disease (Amyloid Peptides 1-38, 1-40, 1-42, Tau Protein, Beclin 1) in the Blood of Neonates after Perinatal Asphyxia

by Agata Tarkowska, Wanda Furmaga-Jabłońska, Jacek Bogucki, Janusz Kocki and Ryszard Pluta

Int. J. Mol. Sci. 2023, 24(17), 13292; https://doi.org/10.3390/ijms241713292 - 27 Aug 2023

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Abstract

Perinatal asphyxia is a complex disease involving massive death of brain cells in full-term newborns. The most impressive consequence of perinatal asphyxia is a neurodegenerative brain injury called hypoxic–ischemic encephalopathy. Management of newborns after perinatal asphyxia is very difficult due to the lack of measurable biomarkers that would be able to assess the severity of the brain injury in the future, help in the selection of therapy, assess the results of treatment and determine the prognosis for the future. Thus, these limitations make long-term neurodevelopmental outcomes unpredictable during life. Quantifying biomarkers that can detect subclinical changes at a stage where routine brain monitoring or imaging is still mute would be a major advance in the care of neonates with brain neurodegeneration after asphyxia. Understanding the effect of perinatal asphyxia on changes in blood neurodegenerative biomarkers over time, which would be commonly used to assess the severity of postpartum encephalopathy, would be an important step in developing precision in predicting the consequences of brain injuries. We urgently need more accurate early predictive markers to guide clinicians when to use neuroprotective therapy. The needed neurodegenerative biomarkers may represent neuronal pathological changes that can be recognized by new technologies such as genomic and proteomic. Nevertheless, the simultaneous blood tau protein and various amyloid changes with the addition of an autophagy marker beclin 1 after perinatal asphyxia have not been studied. We decided to evaluate serum biomarkers of neuronal injury characteristic for Alzheimer’s disease such as amyloid peptides (1-38, 1-40 and 1-42), tau protein and beclin 1, which can predict the progression of brain neurodegeneration in future. In this paper, we report for the first time the significant changes in the above molecules in the blood after asphyxia compared to healthy controls during the 1–7, 8–14 and 15+ days ELISA test. Full article

(This article belongs to the Special Issue Ischemic Genetic Pathology in Neurodegenerative Diseases)

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Review

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25 pages, 1643 KiB

Open AccessReview

Blood and Brain Metabolites after Cerebral Ischemia

by Eva Baranovicova, Dagmar Kalenska, Peter Kaplan, Maria Kovalska, Zuzana Tatarkova and Jan Lehotsky

Int. J. Mol. Sci. 2023, 24(24), 17302; https://doi.org/10.3390/ijms242417302 - 9 Dec 2023

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Abstract

The study of an organism’s response to cerebral ischemia at different levels is essential to understanding the mechanism of the injury and protection. A great interest is devoted to finding the links between quantitative metabolic changes and post-ischemic damage. This work aims to summarize the outcomes of the most studied metabolites in brain tissue—lactate, glutamine, GABA (4-aminobutyric acid), glutamate, and NAA (N-acetyl aspartate)—regarding their biological function in physiological conditions and their role after cerebral ischemia/reperfusion. We focused on ischemic damage and post-ischemic recovery in both experimental—including our results—as well as clinical studies. We discuss the role of blood glucose in view of the diverse impact of hyperglycemia, whether experimentally induced, caused by insulin resistance, or developed as a stress response to the cerebral ischemic event. Additionally, based on our and other studies, we analyze and critically discuss post-ischemic alterations in energy metabolites and the elevation of blood ketone bodies observed in the studies on rodents. To complete the schema, we discuss alterations in blood plasma circulating amino acids after cerebral ischemia. So far, no fundamental brain or blood metabolite(s) has been recognized as a relevant biological marker with the feasibility to determine the post-ischemic outcome or extent of ischemic damage. However, studies from our group on rats subjected to protective ischemic preconditioning showed that these animals did not develop post-ischemic hyperglycemia and manifested a decreased metabolic infringement and faster metabolomic recovery. The metabolomic approach is an additional tool for understanding damaging and/or restorative processes within the affected brain region reflected in the blood to uncover the response of the whole organism via interorgan metabolic communications to the stressful cerebral ischemic challenge. Full article

(This article belongs to the Special Issue Ischemic Genetic Pathology in Neurodegenerative Diseases)

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