Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Ischemic Brain Neurodegeneration 2.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Ischemic Brain Neurodegeneration 2.0

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 November 2022) | Viewed by 8453

Special Issue Editor

Prof. Dr. Ryszard Pluta

E-Mail Website
Guest Editor
Department of Pathophysiology, Medical University of Lublin, 20-612 Lublin, Poland
Interests: brain ischemia; brain ischemia versus Alzheimer's disease; neurodegeneration; amyloid; presenilins; tau protein; autophagy; mitophagy; apoptosis; genes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain ischemia is one of the most common forms of neurodegeneration, with a series of pathological processes that occur mainly post-ischemia and gradually spread to various brain structures. Both ischemic stroke in humans and experimental brain ischemia are life-threatening pathological events with the development of Alzheimer’s disease-type dementia. New data indicate that ischemic processes may be involved in the development of Alzheimer's disease and that there is a similarity between ischemic neuropathology and Alzheimer's disease. First, ischemic stroke and Alzheimer’s disease have the same risk factors. Second, the post-ischemic brain generates a unique pattern of neuronal death in the hippocampus with serious general brain atrophy, which is similar to the atrophy noted in Alzheimer’s disease. Third, neuroinflammatory reactions have an important role in the progress of the post-ischemic brain injury and Alzheimer’s disease. Fourth, data suggest that post-ischemic brain injury may induce neuropathology of folding proteins characteristic of Alzheimer's disease such as amyloid and tau protein. It is suggested that Alzheimer’s disease-related proteins, like amyloid and tau protein, and their genes, play a fundamental role in post-ischemic neuronal death and neurodegeneration. It is, therefore, important to better understand the contribution of neuronal death to neurodegeneration, the molecular and cellular mechanisms leading to neuronal death, and to identify natural or unnatural molecules that can prevent this death. Progress in understanding new key processes induced by brain ischemia, like changes in the genotype and phenotype of the Alzheimer’s disease-type, which are not yet fully explained, may help develop strategies for prevention and treatment post-ischemic neurodegeneration.

Prof. Dr. Ryszard Pluta
Guest Editor

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

  • brain ischemia
  • stroke
  • blood-brain barrier
  • neuroinflammation
  • necrosis
  • apoptosis
  • autophagy
  • mitophagy
  • amyloid
  • Tau protein
  • apolipoproteins
  • presenilins
  • α-synuclein
  • RAGE
  • LRP1
  • gut microbiota
  • dementia
  • therapeutics

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

11 pages, 466 KiB  
Editorial
Acetylated Tau Protein: A New Piece in the Puzzle between Brain Ischemia and Alzheimer’s Disease
by Ryszard Pluta, Sławomir Januszewski and Mirosław Jabłoński
Int. J. Mol. Sci. 2022, 23(16), 9174; https://doi.org/10.3390/ijms23169174 - 16 Aug 2022
Cited by 2 | Viewed by 1694
Abstract
Cerebral ischemia in humans and animals is a life-threatening neuropathological event and leads to the development of dementia with the Alzheimer’s disease phenotype [...] Full article
(This article belongs to the Special Issue Ischemic Brain Neurodegeneration 2.0)
►▼ Show Figures

Figure 1

Research

Jump to: Editorial, Review

14 pages, 5303 KiB  
Article
Validation of the Reference Genes for Expression Analysis in the Hippocampus after Transient Ischemia/Reperfusion Injury in Gerbil Brain
by Anita Lewczuk, Anna Boratyńska-Jasińska and Barbara Zabłocka
Int. J. Mol. Sci. 2023, 24(3), 2756; https://doi.org/10.3390/ijms24032756 - 1 Feb 2023
Cited by 3 | Viewed by 1520
Abstract
Transient brain ischemia in gerbils is a common model to study the mechanisms of neuronal changes in the hippocampus. In cornu ammonnis 2–3, dentate gyrus (CA2-3,DG) regions of the hippocampus, neurons are resistant to 5-min ischemia/reperfusion (I/R) insult, while cornu ammonnis 1 (CA1) [...] Read more.
Transient brain ischemia in gerbils is a common model to study the mechanisms of neuronal changes in the hippocampus. In cornu ammonnis 2–3, dentate gyrus (CA2-3,DG) regions of the hippocampus, neurons are resistant to 5-min ischemia/reperfusion (I/R) insult, while cornu ammonnis 1 (CA1) is found to be I/R-vulnerable. The quantitative polymerase chain reaction (qRT-PCR) is widely used to study the expression of genes involved in these phenomena. It requires stable and reliable genes for normalization, which is crucial for comparable and reproducible analyses of expression changes of the genes of interest. The aim of this study was to determine the best housekeeping gene for the I/R gerbil model in two parts of the hippocampus in controls and at 3, 48, and 72 h after recanalization. We selected and tested six reference genes frequently used in central nervous system studies: Gapdh, Actb, 18S rRNA, Hprt1, Hmbs, Ywhaz, and additionally Bud23, using RefFinder, a comprehensive tool based on four commonly used algorithms: delta cycle threshold (Ct), BestKeeper, NormFinder, and geNorm, while Hprt1 and Hmbs were the most stable ones in CA2-3,DG. Hmbs was the most stable in the whole hippocampal formation. This indicates that the general use of Hmbs, especially in combination with Gapdh, a highly expressed reference gene, seems to be suitable for qRT-PCR normalization in all hippocampal regions in this model. Full article
(This article belongs to the Special Issue Ischemic Brain Neurodegeneration 2.0)
►▼ Show Figures

Graphical abstract

16 pages, 13763 KiB  
Article
Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury
by Choong-Hyun Lee, Tae-Kyeong Lee, Dae Won Kim, Soon Sung Lim, Il Jun Kang, Ji Hyeon Ahn, Joon Ha Park, Jae-Chul Lee, Choong-Hyo Kim, Yoonsoo Park, Moo-Ho Won and Soo Young Choi
Int. J. Mol. Sci. 2022, 23(9), 5096; https://doi.org/10.3390/ijms23095096 - 3 May 2022
Cited by 6 | Viewed by 1752
Abstract
Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can [...] Read more.
Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis. Full article
(This article belongs to the Special Issue Ischemic Brain Neurodegeneration 2.0)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

15 pages, 761 KiB  
Review
Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?
by Ryszard Pluta, Sławomir Januszewski and Stanisław J. Czuczwar
Int. J. Mol. Sci. 2022, 23(12), 6591; https://doi.org/10.3390/ijms23126591 - 13 Jun 2022
Cited by 3 | Viewed by 2767
Abstract
Currently, there is a lot of public interest in naturally occurring substances with medicinal properties that are minimally toxic, readily available and have an impact on health. Over the past decade, molecular hydrogen has gained the attention of both preclinical and clinical researchers. [...] Read more.
Currently, there is a lot of public interest in naturally occurring substances with medicinal properties that are minimally toxic, readily available and have an impact on health. Over the past decade, molecular hydrogen has gained the attention of both preclinical and clinical researchers. The death of pyramidal neurons in especially the CA1 area of the hippocampus, increased permeability of the blood-brain barrier, neuroinflammation, amyloid accumulation, tau protein dysfunction, brain atrophy, cognitive deficits and dementia are considered an integral part of the phenomena occurring during brain neurodegeneration after ischemia. This review focuses on assessing the current state of knowledge about the neuroprotective effects of molecular hydrogen following ischemic brain injury. Recent studies in animal models of focal or global cerebral ischemia and cerebral ischemia in humans suggest that hydrogen has pleiotropic neuroprotective properties. One potential mechanism explaining some of the general health benefits of using hydrogen is that it may prevent aging-related changes in cellular proteins such as amyloid and tau protein. We also present evidence that, following ischemia, hydrogen improves cognitive and neurological deficits and prevents or delays the onset of neurodegenerative changes in the brain. The available evidence suggests that molecular hydrogen has neuroprotective properties and may be a new therapeutic agent in the treatment of neurodegenerative diseases such as neurodegeneration following cerebral ischemia with progressive dementia. We also present the experimental and clinical evidence for the efficacy and safety of hydrogen use after cerebral ischemia. The therapeutic benefits of gas therapy open up new promising directions in breaking the translational barrier in the treatment of ischemic stroke. Full article
(This article belongs to the Special Issue Ischemic Brain Neurodegeneration 2.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop