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Brain Sciences
Special Issues
Precision Medicine and Neurodegenerative Disorders: Past Lessons and New Advances
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Precision Medicine and Neurodegenerative Disorders: Past Lessons and New Advances

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (15 January 2024) | Viewed by 3925

Special Issue Editor

Dr. Wael Mohamed Yousef Mohamed

E-Mail Website
Guest Editor
Department of Basic Medical Sciences, Kulliyyah of Medicine, International Islamic University Malaysia, Kuantan, Malaysia
Interests: Parkinson’s disease; Alzheimer’s dementia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative disorders including AD and PD are complex illness that include genetic, interactome, and environmental factors. Fresh molecular and high-throughput methods are shedding new insight on the pathways and networks at the heart of this complicated diseases. This is required to go forward with the precision medicine paradigm toward novel molecular markers, systematic risk categorization, and translational targeted medicines. The implementation of a complete precision medicine strategy, as well as the creation of relevant biomarkers, are likely to result in significant advancements in recognizing, treating, and preventing neurodegenerative disorders. As a result, after more than a decade of fruitless therapy trials and one of the lowest drug discovery success rates in medicine, the time has come to thoroughly investigate the possibility of employing omics in the treatment of neurodegenerative disorders.

The present collection spans from basic research to clinical/ neuropathological studies, with an aim to instigate novel approaches towards the understanding, diagnosing and treatment of NDG disorders. We encourage submission of original empirical research articles. Furthermore, the call is open for theoretical approaches such as Reviews, Perspective, and Opinion articles on promising future directions. This Research Topic is widely open to contributions that target the following topics:

1-Hallmarks of CNS aging (genetic factors, epigenetic signatures, telomeres,…).

2-Detection of specific cell type marker genes for aging.

3-Finding the altered genes with NDG disorders.

4-Quantifying changes of different cell types in NDG disorders

5-Finding possible changes in molecular pathways in NDG disorders (e.g., signalling pathways, inflammation, alternative splicing).

6-Exploring novel cell markers that have altered expression in brain aging and NDG disorders.

7-In-depth analysis of the changes in alternative splicing in aging brain such as a comparison with additional external expression datasets (e.g., RNA-seq, from the Gene Expression Omnibus).

8-Review and perspective articles that discuss recent advances, potential contexts of use and future perspectives of genetic biomarkers in NDG disorders.

9-Animal models for studying NDG disorders.

10-Translational neuroscience research that addresses various unsolved issues in NDG disorders.

11-Researches that focus on new neuroscience disciplines like stem cell, neurotechnology (imaging, tractography, telemedicine…), personalized medicine,…etc.

Dr. Wael Mohamed Yousef Mohamed
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. Brain Sciences 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 2200 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

  • neurodegenerative disorders
  • dementia
  • precision medicine
  • biomarkers
  • aging
  • PD

Published Papers (2 papers)

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Research

15 pages, 2409 KiB  
Article
Mitophagy: A Bridge Linking HMGB1 and Parkinson’s Disease Using Adult Zebrafish as a Model Organism
by Khairiah Razali, Mohd Hamzah Mohd Nasir, Jaya Kumar and Wael M. Y. Mohamed
Brain Sci. 2023, 13(7), 1076; https://doi.org/10.3390/brainsci13071076 - 16 Jul 2023
Viewed by 1357
Abstract
High-mobility group box 1 (HMGB1) has been implicated as a key player in two critical factors of Parkinson’s disease (PD): mitochondrial dysfunction and neuroinflammation. However, the specific role of HMGB1 in PD remains elusive. We investigated the effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration on [...] Read more.
High-mobility group box 1 (HMGB1) has been implicated as a key player in two critical factors of Parkinson’s disease (PD): mitochondrial dysfunction and neuroinflammation. However, the specific role of HMGB1 in PD remains elusive. We investigated the effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration on mitochondrial dysfunction and HMGB1-associated inflammatory genes as well as locomotor activity in zebrafish, aiming to elucidate the role of HMGB1 in PD. Adult zebrafish received MPTP injections, and locomotor activity was measured at 24- and 48-h post-administration. Gene expression levels related to mitophagy (fis1, pink1, and park2) and HMGB1-mediated inflammation (hmgb1, tlr4, and nfkb) were quantified through RT-qPCR analysis. Following MPTP injection, the significant increase in transcript levels of fis1, pink1, and park2 indicated notable changes in PINK1/Parkin mitophagy, while the upregulation of hmgb1, tlr4, and nfkb genes pointed to the activation of the HMGB1/TLR4/NFκB inflammatory pathway. Furthermore, MPTP-injected zebrafish exhibited decreased locomotor activity, evident through reduced distance travelled, mean speed, and increased freezing durations. HMGB1 plays a major role in cellular processes as it is involved in both the mitophagy process and functions as a pro-inflammatory protein. MPTP administration in adult zebrafish activated mitophagy and inflammatory signaling, highlighting the significant role of HMGB1 as a mediator in both processes and further emphasizing its significant contribution to PD pathogenesis. Full article
(This article belongs to the Special Issue Precision Medicine and Neurodegenerative Disorders: Past Lessons and New Advances)
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12 pages, 3989 KiB  
Article
A Transgenic 5xFAD-M Line of Mice for Dendritic Spine Morphology Analysis in Alzheimer’s Disease
by Anastasiia Ilina and Natalia Linkova
Brain Sci. 2023, 13(2), 307; https://doi.org/10.3390/brainsci13020307 - 10 Feb 2023
Viewed by 1837
Abstract
Cognitive impairments are closely related to synaptic loss in Alzheimer’s disease (AD). Functional changes in synaptic contacts are reflected in dendritic spine morphology. Visualization of neurons for morphological studies in vivo is complicated by the fixed brain slice staining or expensive adeno-associated virus [...] Read more.
Cognitive impairments are closely related to synaptic loss in Alzheimer’s disease (AD). Functional changes in synaptic contacts are reflected in dendritic spine morphology. Visualization of neurons for morphological studies in vivo is complicated by the fixed brain slice staining or expensive adeno-associated virus injections. We created a transgenic 5xFAD-M line of mice with AD-associated mutations and expressed GFP protein in single neurons of the brain. This mouse model of AD is a useful tool for the simplified visualization of the hippocampal neurons’ morphology in vivo without additional staining manipulations. The progressive elimination of mushroom spines was demonstrated in 5xFAD-M mice between 4 and 5 months of age. Five-month-old 5xFAD-M male and female mice showed change both in the total density and the mushroom spines number compared to sex-matched control. We conclude 5xFAD-M mice can be a useful AD model for studying the mechanisms of synaptic pathology under neurodegenerative conditions and evaluating the effects of potential therapeutic agents on spine morphology as crucial aspect of memory loss in AD. Full article
(This article belongs to the Special Issue Precision Medicine and Neurodegenerative Disorders: Past Lessons and New Advances)
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