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Editorial Board Members’ Collection Series: “Molecular Research in Alzheimer’s Disease”

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: 30 April 2024 | Viewed by 370

Special Issue Editors


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Guest Editor
1. Department of Neurology, University Hospital “12 de Octubre”, 28041 Madrid, Spain
2. Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 28029 Madrid, Spain
3. Department of Medicine, Complutense University, 28040 Madrid, Spain
Interests: neurodegenerative diseases; pathogenesis; neuroepidemiology
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Harrison College of Pharmacy, Department of Drug Discovery and Development, Auburn University, Auburn, AL 36849, USA
Interests: Alzheimer's disease; cerebral amyloid angiopathy; blood-brain barrier; neuroinflammation; amyloid-beta
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Pharmacology Section, Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institute of Neuroscience, Universitat de Barcelona, 08028 Barcelona, Spain
Interests: ageing; neurodegeneration; alzheimer's disease; neuropharmacology; oxidative stress; mitochondria; proteostasis; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The collection “Molecular Research in Alzheimer’s disease” in the International Journal of Molecular Sciences (IJMS) offers a comprehensive review of cutting-edge studies addressing the molecular underpinnings of Alzheimer’s Disease (AD). Alzheimer’s, a devastating neurodegenerative disorder, presents complex multifactorial etiologies, and this series sheds light on the intricate interplay of the genetic, proteomic, and metabolic pathways implicated in its pathogenesis. This collection unveils potential therapeutic targets by exploring the role of beta-amyloid accumulation, tau protein phosphorylation, neuroinflammation, and oxidative stress. Furthermore, it delves into novel biomarkers for early AD diagnosis, providing a beacon of hope for timely interventions. The featured studies harness advanced molecular techniques, from genomic sequencing to proteomic analyses, underscoring the importance of a multidisciplinary approach to decipher the complexities of AD. This series is a pivotal resource for researchers, clinicians, and students, facilitating a deeper understanding of AD’s molecular landscape and driving innovative diagnosis, prevention, and treatment strategies. Through this compilation, the IJMS Editorial Board Members reiterate the significance of molecular research in shaping the future landscape of AD management.

Dr. Julián Benito-León
Prof. Dr. Amal Kaddoumi
Prof. Dr. Mercè Lliberia
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

  • Alzheimer’s disease (AD)
  • molecular underpinnings
  • neurodegenerative disorder
  • beta-amyloid accumulation
  • tau protein phosphorylation
  • neuroinflammation
  • oxidative stress
  • therapeutic targets
  • biomarkers
  • early diagnosis
  • genomic sequencing
  • proteomic analyses
  • multidisciplinary approach
  • prevention
  • treatment

Published Papers (1 paper)

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Research

22 pages, 2630 KiB  
Article
Dual Role of NMDAR-Containing NR2A and NR2B Subunits in Alzheimer’s Disease
by Iu Raïch, Jaume Lillo, Joan Biel Rebassa, Toni Capó, Arnau Cordomí, Irene Reyes-Resina, Mercè Pallàs and Gemma Navarro
Int. J. Mol. Sci. 2024, 25(9), 4757; https://doi.org/10.3390/ijms25094757 (registering DOI) - 26 Apr 2024
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Abstract
Alzheimer’s disease (AD) is the main cause of dementia worldwide. Given that learning and memory are impaired in this pathology, NMDA receptors (NMDARs) appear as key players in the onset and progression of the disease. NMDARs are glutamate receptors, mainly located at the [...] Read more.
Alzheimer’s disease (AD) is the main cause of dementia worldwide. Given that learning and memory are impaired in this pathology, NMDA receptors (NMDARs) appear as key players in the onset and progression of the disease. NMDARs are glutamate receptors, mainly located at the post-synapse, which regulate voltage-dependent influx of calcium into the neurons. They are heterotetramers, and there are different subunits that can be part of the receptors, which are usually composed of two obligatory GluN1 subunits plus either two NR2A or two NR2B subunits. NR2A are mostly located at the synapse, and their activation is involved in the expression of pro-survival genes. Conversely, NR2B are mainly extrasynaptic, and their activation has been related to cell death and neurodegeneration. Thus, activation of NR2A and/or inactivation of NR2B-containing NMDARS has been proposed as a therapeutic strategy to treat AD. Here, we wanted to investigate the main differences between both subunits signalling in neuronal primary cultures of the cortex and hippocampus. It has been observed that Aβ induces a significant increase in calcium release and also in MAPK phosphorylation signalling in NMDAR-containing NR2B subunits in cortical and hippocampal neurons. However, while NMDAR-containing NR2A decreases neuronal death and favours cell viability after Aβ treatment, NMDAR-containing NR2B shows higher levels of cytotoxicity and low levels of neuronal survival. Finally, it has been detected that NMDAR has no effect on pTau axonal transport. The present results demonstrate a different role between GluNA and GluNB subunits in neurodegenerative diseases such as Alzheimer’s. Full article
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