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Dementia and Cell Theraputic Strategies

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 December 2021) | Viewed by 11250

Special Issue Editors

Division of Integrated Pharmaceutical Sciences, Kyoto Pharmaceutical University, Kyoto, Japan
Interests: aging; neurodegenerative diseases; brain immunity; microglia; stem cells; hematopoietic stem cells; regenerative medicine; pharmacological modification
Molecular Neuroscience Research Center, Shiga University of Medical Science, Shiga, Japan
Interests: Alzheimer’s disease; tauopathy; molecular imaging; protein aggregation; neurodegeneration; biomarker; disease-modifying therapy

Special Issue Information

Dear Colleagues,

It is estimated that 130 million people worldwide will suffer from dementia by 2050. Alzheimer's disease is the most common form of dementia, and there are many brain disorders that lead to the development of dementia (e.g., Lewy body disease), including Parkinson's disease, cerebrovascular disease, Down's syndrome, and Huntington’s disease. Cell therapeutic strategies are an attractive approach to recovering lost brain function. In fact, the improvement of motor function in Parkinson's disease is vigorously promoted by this strategy, and clinical study is now ongoing. Meanwhile, regarding cell therapeutic strategies for recovery of cognitive functions, preclinical studies have been under examination and/or recently launched to establish the proof of concept. The preclinical studies include not only the evaluation of their effectiveness but also the biology of stem cells; development of technologies for production and tracing of therapeutic cells; elucidation of therapeutic mechanism; and application of materials that support survival, function, and safety of therapeutic cells. Contributions to this Special Issue will provide new insights into the possibility of the development of cell-based disease-modifying therapy and the understanding of the pathogenesis of dementia.

Prof. Dr. Kazuyuki Takata
Dr. Daijiro Yanagisawa
Guest Editors

Manuscript Submission Information

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Keywords

  • Alzheimer’s disease
  • amyloid-β
  • tau
  • neurodegeneration
  • neuroinflammation
  • neurons
  • glial cells
  • stem cells
  • Parkinson’s disease
  • Down syndrome
  • regeneration

Published Papers (4 papers)

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Research

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15 pages, 3554 KiB  
Article
Effect of Progranulin on Proliferation and Differentiation of Neural Stem/Progenitor Cells after Oxygen/Glucose Deprivation
by Ichiro Horinokita, Hideki Hayashi, Takamasa Nagatomo, Yuna Fushiki, Yui Iwatani and Norio Takagi
Int. J. Mol. Sci. 2022, 23(4), 1949; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23041949 - 09 Feb 2022
Cited by 4 | Viewed by 1962
Abstract
We previously demonstrated that sivelestat, a selective neutrophil elastase inhibitor, attenuates the cleavage of progranulin (PGRN) and ischemia-induced cell injury in the brain. To obtain further insight into the role of PGRN, in the present study we evaluated the direct effects of sivelestat [...] Read more.
We previously demonstrated that sivelestat, a selective neutrophil elastase inhibitor, attenuates the cleavage of progranulin (PGRN) and ischemia-induced cell injury in the brain. To obtain further insight into the role of PGRN, in the present study we evaluated the direct effects of sivelestat and recombinant PGRN (rPGRN) on the proliferation and differentiation of neural stem cells in cultures of neural stem/progenitor cells (NS/PC) under the ischemic condition in vitro. We demonstrated that oxygen/glucose deprivation (OGD)-induced cell proliferation of NS/PC was increased by rPGRN treatment. In addition, this increase was accompanied by increased phosphorylation of Akt and GSK-3β (Ser9) after OGD. But none of these responses occurred by treatment with sivelestat. Therefore, activation of the Akt/GSK-3β pathway could well be involved in this proliferative effect of rPGRN. Although OGD and reoxygenation-induced changes in the differentiation of NS/PC into neurons or astrocytes was not affected by treatment with rPGRN or sivelestat, it is noteworthy that rPGRN enhanced neurite outgrowth of β3-tubulin-positive neurons that had differentiated from the NS/PC. These findings suggest that enhancement of proliferation of endogenous NS/PC and neurite outgrowth of differentiated neurons from NS/PC by PGRN could be useful for a new therapeutic approach for cerebral ischemia. Full article
(This article belongs to the Special Issue Dementia and Cell Theraputic Strategies)
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13 pages, 3605 KiB  
Article
Kaempferol Has Potent Protective and Antifibrillogenic Effects for α-Synuclein Neurotoxicity In Vitro
by Masatoshi Inden, Ayaka Takagi, Hazuki Kitai, Taisei Ito, Hisaka Kurita, Ryo Honda, Yuji O. Kamatari, Sora Nozaki, Xiaopeng Wen, Masanori Hijioka, Yoshihisa Kitamura and Isao Hozumi
Int. J. Mol. Sci. 2021, 22(21), 11484; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111484 - 25 Oct 2021
Cited by 16 | Viewed by 2066
Abstract
Aggregation of α-synuclein (α-Syn) is implicated in the pathogenesis of Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Therefore, the removal of α-Syn aggregation could lead to the development of many new therapeutic agents for neurodegenerative diseases. In [...] Read more.
Aggregation of α-synuclein (α-Syn) is implicated in the pathogenesis of Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Therefore, the removal of α-Syn aggregation could lead to the development of many new therapeutic agents for neurodegenerative diseases. In the present study, we succeeded in generating a new α-Syn stably expressing cell line using a piggyBac transposon system to investigate the neuroprotective effect of the flavonoid kaempferol on α-Syn toxicity. We found that kaempferol provided significant protection against α-Syn-related neurotoxicity. Furthermore, kaempferol induced autophagy through an increase in the biogenesis of lysosomes by inducing the expression of transcription factor EB and reducing the accumulation of α-Syn; thus, kaempferol prevented neuronal cell death. Moreover, kaempferol directly blocked the amyloid fibril formation of α-Syn. These results support the therapeutic potential of kaempferol in diseases such as synucleinopathies that are characterized by α-Syn aggregates. Full article
(This article belongs to the Special Issue Dementia and Cell Theraputic Strategies)
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Review

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12 pages, 642 KiB  
Review
Combination of Drugs and Cell Transplantation: More Beneficial Stem Cell-Based Regenerative Therapies Targeting Neurological Disorders
by Kaneyasu Nishimura and Kazuyuki Takata
Int. J. Mol. Sci. 2021, 22(16), 9047; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22169047 - 22 Aug 2021
Cited by 8 | Viewed by 3056
Abstract
Cell transplantation therapy using pluripotent/multipotent stem cells has gained attention as a novel therapeutic strategy for treating neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, ischemic stroke, and spinal cord injury. To fully realize the potential of cell transplantation therapy, new therapeutic [...] Read more.
Cell transplantation therapy using pluripotent/multipotent stem cells has gained attention as a novel therapeutic strategy for treating neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, ischemic stroke, and spinal cord injury. To fully realize the potential of cell transplantation therapy, new therapeutic options that increase cell engraftments must be developed, either through modifications to the grafted cells themselves or through changes in the microenvironment surrounding the grafted region. Together these developments could potentially restore lost neuronal function by better supporting grafted cells. In addition, drug administration can improve the outcome of cell transplantation therapy through better accessibility and delivery to the target region following cell transplantation. Here we introduce examples of drug repurposing approaches for more successful transplantation therapies based on preclinical experiments with clinically approved drugs. Drug repurposing is an advantageous drug development strategy because drugs that have already been clinically approved can be repurposed to treat other diseases faster and at lower cost. Therefore, drug repurposing is a reasonable approach to enhance the outcomes of cell transplantation therapies for neurological diseases. Ideal repurposing candidates would result in more efficient cell transplantation therapies and provide a new and beneficial therapeutic combination. Full article
(This article belongs to the Special Issue Dementia and Cell Theraputic Strategies)
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15 pages, 1174 KiB  
Review
The Role of PERK in Understanding Development of Neurodegenerative Diseases
by Garrett Dalton Smedley, Keenan E. Walker and Shauna H. Yuan
Int. J. Mol. Sci. 2021, 22(15), 8146; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158146 - 29 Jul 2021
Cited by 12 | Viewed by 3573
Abstract
Neurodegenerative diseases are an ever-increasing problem for the rapidly aging population. Despite this, our understanding of how these neurodegenerative diseases develop and progress, is in most cases, rudimentary. Protein kinase RNA (PKR)-like ER kinase (PERK) comprises one of three unfolded protein response pathways [...] Read more.
Neurodegenerative diseases are an ever-increasing problem for the rapidly aging population. Despite this, our understanding of how these neurodegenerative diseases develop and progress, is in most cases, rudimentary. Protein kinase RNA (PKR)-like ER kinase (PERK) comprises one of three unfolded protein response pathways in which cells attempt to manage cellular stress. However, because of its role in the cellular stress response and the far-reaching implications of this pathway, error within the PERK pathway has been shown to lead to a variety of pathologies. Genetic and clinical studies show a correlation between failure of the PERK pathway in neural cells and the development of neurodegeneration, but the wide array of methodology of these studies is presenting conflicting narratives about the role of PERK in these affected systems. Because of the connection between PERK and pathology, PERK has become a high value target of study for understanding neurodegenerative diseases and potentially how to treat them. Here, we present a review of the literature indexed in PubMed of the PERK pathway and some of the complexities involved in investigating the protein’s role in the development of neurodegenerative diseases as well as how it may act as a target for therapeutics. Full article
(This article belongs to the Special Issue Dementia and Cell Theraputic Strategies)
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