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Disease Modifying Translational Research for Neurological Disorders and Brain Damages
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Disease Modifying Translational Research for Neurological Disorders and Brain Damages

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 2022) | Viewed by 10047

Special Issue Editors

Prof. Dr. Yunjong Lee

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Guest Editor
Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Korea
Interests: Parkinson’s disease; Animal model; High throughput screening; Diagnostic biomarkers; Neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Seung Pil Yun

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Guest Editor
Department of Pharmacology, School of Medicine, Gyeongsang National University, 15 Jinjudae-ro 816, Jinju 52727, Korea
Interests: Neuro-iflammation; Neurodegenrative disease; Stem cell application for brain: Relationship CNS and peripheral organ inflammation; Brain cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Age-related neurodegenerative brain disorders and acute brain injuries are great medical challenges with no effective disease-modifying therapies. Currently available therapies are mainly centered on mitigating clinical symptoms. However, these symptomatic treatments have failed to control fundamental aspects of many brain diseases. Neurological disorders oftentimes involve not only pathological alterations within the affected neurons themselves but also unfavorable surrounding environments, thereby suggesting diverse therapeutic targets. Moreover, advanced biotechnologies have enabled us to come up with more revealing cellular and animal model systems with great flexibility in translational research.

In this regard, the aim of this Special Issue is to provide diverse translational approaches (as the format of original research articles or reviews) targeting brain-disease-associated pathological cells and molecular pathways by employing cellular and animal models of brain disorders. This Special Issue also welcomes translational and basic research on cell and animal model development which can be effectively used for high-throughput screening or preclinical studies. 

Prof. Dr. Yunjong Lee
Prof. Dr. Seung Pil Yun
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

  • Neurodegenerative disease
  • Stroke and ischemia
  • Disease modeling
  • Neuroinflammation
  • Disease-modifying therapy
  • Small molecules
  • Natural compounds
  • Biologics
  • Preclinical study
  • High-throughput screen

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Published Papers (3 papers)

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Research

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16 pages, 5091 KiB  
Article
Synthetic Peucedanocoumarin IV Prevents α-Synuclein Neurotoxicity in an Animal Model of Parkinson’s Disease
by Heejeong Kim, Han-Joo Maeng, Ji Hun Kim, Jin-Ha Yoon, Yohan Oh, Seung-Mann Paek and Yunjong Lee
Int. J. Mol. Sci. 2022, 23(15), 8618; https://doi.org/10.3390/ijms23158618 - 3 Aug 2022
Cited by 4 | Viewed by 2335
Abstract
Pathological protein inclusion formation and propagation are the main causes of neuronal dysfunction in diverse neurodegenerative diseases; therefore, current disease-modifying therapeutic strategies have targeted this disease protein aggregation process. Recently, we reported that peucedanocoumarin III (PCiii) is a promising therapeutic compound with the [...] Read more.
Pathological protein inclusion formation and propagation are the main causes of neuronal dysfunction in diverse neurodegenerative diseases; therefore, current disease-modifying therapeutic strategies have targeted this disease protein aggregation process. Recently, we reported that peucedanocoumarin III (PCiii) is a promising therapeutic compound with the ability to disaggregate α-synuclein inclusion and protect dopaminergic neurons in Parkinson’s disease (PD). Here, we found that trans-4′-acetyl-3′-tigloylkhellactone (racemic peucedanocoumarin IV [PCiv]), a structural isomer of PCiii with a higher synthetic yield presented a strong anti-aggregate activity to a degree comparable to that of PCiii. PCiv retained effective inhibitory function against β-sheet aggregate-mimic β23 cytotoxicities and potently prevented α-synucleinopathy in α-synuclein preformed fibril (PFF)-treated mice cortical neurons. In detailed pharmacokinetic profiling of PCiv, oral administration of PCiv in rats exhibited an approximately 97-min half-life and 10% bioavailability. Moreover, tissue distribution analysis revealed favorable profiles of brain penetration with a 6.4 brain-to-plasma concentration ratio. The therapeutic efficacy of PCiv was further evaluated in a sporadic PD mouse model with a combinatorial co-injection of α-synuclein preformed fibril and recombinant adeno-associated virus expressing α-synuclein. Motor dysfunctions induced in this combinatorial α-synucleinopathy PD mouse model was almost completely rescued by PCiv diet administration, and this therapeutic effect is consistent with the marked prevention of dopaminergic neuron loss and suppression of α-synuclein aggregation. Taken together, our translational study suggests that PCiv is advantageous as a therapeutic agent for neurodegenerative diseases, especially with its good synthetic yield, high brain distribution, and anti-aggregate activity. PCiv may be useful in the management of α-synuclein inclusion formation and propagation at different stages of PD. Full article
(This article belongs to the Special Issue Disease Modifying Translational Research for Neurological Disorders and Brain Damages)
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33 pages, 5624 KiB  
Article
Modelling the Human Blood–Brain Barrier in Huntington Disease
by Domenico Vignone, Odalys Gonzalez Paz, Ivan Fini, Antonella Cellucci, Giulio Auciello, Maria Rosaria Battista, Isabelle Gloaguen, Silvia Fortuni, Cristina Cariulo, Vinod Khetarpal, Celia Dominguez, Ignacio Muñoz-Sanjuán and Annalise Di Marco
Int. J. Mol. Sci. 2022, 23(14), 7813; https://doi.org/10.3390/ijms23147813 - 15 Jul 2022
Cited by 7 | Viewed by 2990
Abstract
While blood–brain barrier (BBB) dysfunction has been described in neurological disorders, including Huntington’s disease (HD), it is not known if endothelial cells themselves are functionally compromised when promoting BBB dysfunction. Furthermore, the underlying mechanisms of BBB dysfunction remain elusive given the limitations with [...] Read more.
While blood–brain barrier (BBB) dysfunction has been described in neurological disorders, including Huntington’s disease (HD), it is not known if endothelial cells themselves are functionally compromised when promoting BBB dysfunction. Furthermore, the underlying mechanisms of BBB dysfunction remain elusive given the limitations with mouse models and post mortem tissue to identify primary deficits. We established models of BBB and undertook a transcriptome and functional analysis of human induced pluripotent stem cell (iPSC)-derived brain-like microvascular endothelial cells (iBMEC) from HD patients or unaffected controls. We demonstrated that HD-iBMECs have abnormalities in barrier properties, as well as in specific BBB functions such as receptor-mediated transcytosis. Full article
(This article belongs to the Special Issue Disease Modifying Translational Research for Neurological Disorders and Brain Damages)
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Review

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33 pages, 2133 KiB  
Review
Disease-Modifying Effects of Non-Invasive Electroceuticals on β-Amyloid Plaques and Tau Tangles for Alzheimer’s Disease
by Junsoo Bok, Juchan Ha, Bum Ju Ahn and Yongwoo Jang
Int. J. Mol. Sci. 2023, 24(1), 679; https://doi.org/10.3390/ijms24010679 - 30 Dec 2022
Cited by 7 | Viewed by 3949
Abstract
Electroceuticals refer to various forms of electronic neurostimulators used for therapy. Interdisciplinary advances in medical engineering and science have led to the development of the electroceutical approach, which involves therapeutic agents that specifically target neural circuits, to realize precision therapy for Alzheimer’s disease [...] Read more.
Electroceuticals refer to various forms of electronic neurostimulators used for therapy. Interdisciplinary advances in medical engineering and science have led to the development of the electroceutical approach, which involves therapeutic agents that specifically target neural circuits, to realize precision therapy for Alzheimer’s disease (AD). To date, extensive studies have attempted to elucidate the disease-modifying effects of electroceuticals on areas in the brain of a patient with AD by the use of various physical stimuli, including electric, magnetic, and electromagnetic waves as well as ultrasound. Herein, we review non-invasive stimulatory systems and their effects on β-amyloid plaques and tau tangles, which are pathological molecular markers of AD. Therefore, this review will aid in better understanding the recent technological developments, applicable methods, and therapeutic effects of electronic stimulatory systems, including transcranial direct current stimulation, 40-Hz gamma oscillations, transcranial magnetic stimulation, electromagnetic field stimulation, infrared light stimulation and ionizing radiation therapy, and focused ultrasound for AD. Full article
(This article belongs to the Special Issue Disease Modifying Translational Research for Neurological Disorders and Brain Damages)
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