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Life
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Revolutionizing Neuroregeneration
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Revolutionizing Neuroregeneration

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3466

Special Issue Editor

Prof. Dr. Kiminobu Sugaya

E-Mail Website
Guest Editor
College of Medicine, University of Central Florida, Orlando, FL 32816, USA
Interests: stem cell; Alzheimer’s disease; neurodegenerative diseases; down syndrome; regeneration therapy; cancer stem cell; exosome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The neurodegenerative disease therapies on the market today are symptomatic treatments. Many pharmaceutical companies have tried to develop a cure for Alzheimer’s disease by focusing on immunotherapy and other forms of therapy to eliminate Aβ deposition. However, to date, these efforts to prevent plaque formation have failed to benefit patients, even after investments of billions of dollars. There is a need to establish a new treatment method from an entirely different perspective.

We have known for some time that neural stem cell (NSC) transplantation can improve cognition in aged animals. However, it is challenging to obtain NSCs for transplantation, as they are localized deep in the brain. We have developed technologies to produce pluripotent stem cells from somatic cells, allowing us to use autologous stem cells for transplantation. However, there is still the issue of controlling cell fate and the development of tumors. Thus, we believe that it will take more time for cell-transplantation-based neuroregenerative therapy to be rolled out and become a key part of medicine.

In this Special Issue, we would like to cover new concepts in neuroregeneration therapies, including, but not limited to, using small molecular compounds to increase neurogenesis. We welcome submissions not only of research articles but also of scientific perspectives and comprehensive reviews.

Prof. Dr. Kiminobu Sugaya
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. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • Alzheimer’s disease
  • Parkinson’s disease
  • neuroregeneration
  • stroke
  • regenerative therapy

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Published Papers (3 papers)

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Research

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15 pages, 2660 KiB  
Article
Integrin β2 Plays a Significant Role in Therapeutic Angiogenesis Through Hematopoietic Stem Cell Transplantation
by Orie Saino, Yuko Ogawa, Kazuta Yasui, Akihiro Fuchizaki, Rie Akamatsu, Yoriko Irie, Mitsunobu Tanaka, Takafumi Kimura and Akihiko Taguchi
Life 2025, 15(2), 195; https://doi.org/10.3390/life15020195 - 28 Jan 2025
Viewed by 843
Abstract
The efficacy of hematopoietic stem cell (HSC) therapy for cerebral infarction has been previously demonstrated. However, the lack of response in some patients has hindered its widespread use. To establish HSC therapy as a standard treatment, it is important to examine the causes [...] Read more.
The efficacy of hematopoietic stem cell (HSC) therapy for cerebral infarction has been previously demonstrated. However, the lack of response in some patients has hindered its widespread use. To establish HSC therapy as a standard treatment, it is important to examine the causes of non-responsiveness. In this study, we aimed to identify the specifications of transplanted cells based on their therapeutic mechanisms to predict treatment success. We found that HSC therapy activates injured cerebral endothelial cells via gap junctions because cell adhesion between HSCs and the endothelium plays an essential role in cellular communication via gap junctions. The expression of the adhesion molecule integrin β2 (CD18) in CD34-positive (CD34+) cells was identified as critical for the therapeutic effect on cerebral infarction in a murine model. Cells with low CD18 expression exhibited a weaker therapeutic effect than cells with high CD18 expression, even when the same number of HSCs was administered. The expression of CD18 in CD34+ cells can be used as a specification marker for transplanted HSCs and is useful for identifying non-responders. Furthermore, quantification of CD18 expression is crucial for evaluating the cellular potential of cell-based therapies for diseases where therapeutic effects are mediated through cell adhesion. Full article
(This article belongs to the Special Issue Revolutionizing Neuroregeneration)
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Review

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27 pages, 4424 KiB  
Review
DNA Methylation in Urine and Feces Indicative of Eight Major Human Cancer Types Globally
by Melanie Engstrom Newell, Ayesha Babbrah, Anumitha Aravindan, Raj Rathnam and Rolf U. Halden
Life 2025, 15(3), 482; https://doi.org/10.3390/life15030482 - 17 Mar 2025
Viewed by 757
Abstract
Toxic chemicals and epigenetic biomarkers associated with cancer have been used successfully in clinical diagnostic screening of feces and urine from individuals, but they have been underutilized in a global setting. We analyzed peer-reviewed literature to achieve the following: (i) compile epigenetic biomarkers [...] Read more.
Toxic chemicals and epigenetic biomarkers associated with cancer have been used successfully in clinical diagnostic screening of feces and urine from individuals, but they have been underutilized in a global setting. We analyzed peer-reviewed literature to achieve the following: (i) compile epigenetic biomarkers of disease, (ii) explore whether research locations are geographically aligned with disease hotspots, and (iii) determine the potential for tracking disease-associated epigenetic biomarkers. Studies (n = 1145) of epigenetic biomarkers (n = 146) in urine and feces from individuals have established notable diagnostic potential for detecting and tracking primarily gastric and urinary cancers. Panels with the highest sensitivity and specificity reported more than once were SEPT9 (78% and 93%, respectively) and the binary biomarker combinations GDF15, TMEFF2, and VIM (93% and 95%), NDRG4 and BMP3 (98% and 90%), and TWIST1 and NID2 (76% and 79%). Screening for epigenetic biomarkers has focused on biospecimens from the U.S., Europe, and East Asia, whereas data are limited in regions with similar/higher disease incidence rates (i.e., data for New Zealand, Japan, and Australia for colorectal cancer). The epigenetic markers discussed here may aid in the future monitoring of multiple cancers from individual- to population-level scales by leveraging the emerging science of wastewater-based epidemiology (WBE). Full article
(This article belongs to the Special Issue Revolutionizing Neuroregeneration)
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13 pages, 526 KiB  
Review
Potential Regulation of the Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript1 by Estrogen in Parkinson’s Disease
by Eman Adel and Maya Nicolas
Life 2024, 14(12), 1662; https://doi.org/10.3390/life14121662 - 16 Dec 2024
Viewed by 1156
Abstract
Parkinson’s disease (PD) is the second-leading cause of death among neurodegenerative disease after Alzheimer’s disease (AD), affecting around 2% of the population. It is expected that the incidence of PD will exceed 12 million by 2040. Meanwhile, there is a recognized difference in [...] Read more.
Parkinson’s disease (PD) is the second-leading cause of death among neurodegenerative disease after Alzheimer’s disease (AD), affecting around 2% of the population. It is expected that the incidence of PD will exceed 12 million by 2040. Meanwhile, there is a recognized difference in the phenotypical expression of the disease and response to treatment between men and women. Men have twice the incidence of PD compared to women, who have a late onset and worse prognosis that is usually associated with menopause. In addition, the incidence of PD in women is associated with the cumulative estrogen levels in their bodies. These differences are suggested to be due to the protective effect of estrogen on the brain, which cannot be given in clinical practice to improve the symptoms of the disease because of its peripheral side effects, causing cancer in both males and females in addition to the feminizing effect it has on males. As PD pathophysiology involves alteration in the expression levels of multiple LncRNAs, including metastatic-associated lung adenocarcinoma transcript 1 (MALAT1), and as estrogen has been illustrated to control the expression of MALAT1 in multiple conditions, it is worth investigating the estrogen–MALAT1 interaction in Parkinson’s disease to mimic its protective effect on the brain while avoiding its peripheral side effects. The following literature review suggests the potential regulation of MALAT1 by estrogen in PD, which would enhance our understanding of the pathophysiology of the disease, improving the development of more tailored and effective treatments. Full article
(This article belongs to the Special Issue Revolutionizing Neuroregeneration)
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