Biomolecular Approaches and Drugs for Neurodegeneration—2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 264

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Istituto di Biostrutture e Bioimmagini IBB-CNR, Via Tommaso De Amicis 95, 80145 Naples, Italy
Interests: pharmaceutical chemistry; neurodrugs; protein interactions; spectroscopy; computational chemistry; phytochemistry
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Special Issue Information

Dear Colleagues,

Neuropathologies are very common and disabling conditions affecting the ever-growing elderly population around the world, especially in Western countries. There is an urgent need to develop effective therapies to prevent or treat neuropathologies. Protein/peptide aggregation is of fundamental importance in therapeutics because this type of event is related to pathologies of enormous social relevance, including neurodegeneration. Interestingly, G-quadruplex (G4) DNA and RNA structures are also related to several neuropathologies, and ligands that can destabilize or modulate the aggregation of these nucleic acid secondary structures have therefore been proposed as having the potential to work as neurodrugs. In this Special Issue, we will focus on current experimental and theoretical approaches to neurodrug design and development, with a particular focus on the mechanisms underlying drug interference with protein and peptide aggregation pathways; however, contributions on G4 nucleic acid–drug interactions, G4 targets in neurodegenerative diseases, and nucleopeptide chemistry are also welcome, as they could improve our overall knowledge of the aggregation-based biochemistry at the interface between neurodrug design and therapy. Other themes of interest include applications of computational chemistry and machine learning to chemistry and biology in the context of neuropathology therapy. For this Special Issue, we welcome submissions of original articles and reviews that discuss research and ideas on the theme of neurodegeneration-related molecular strategies.

Dr. Caterina Vicidomini
Dr. Giovanni N. Roviello
Guest Editors

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Keywords

  • proteins
  • peptides
  • amyloid
  • Alzheimer disease
  • Parkinson’s disease
  • neurodrugs
  • G-quadruplex nucleic acids
  • biotechnology
  • biomolecular targets
  • peptide aggregation
  • natural products
  • synthetic drugs
  • anti-amyloid therapeutics
  • machine learning

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Published Papers (1 paper)

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Research

16 pages, 3419 KiB  
Article
[18F]Mefway: Imaging Serotonin 5HT1A Receptors in Human Postmortem Alzheimer’s and Parkinson’s Disease Anterior Cingulate. Potential Applications to Human Positron Emission Tomography Studies
by Noresa L. Gonzaga, Fariha Karim, Christopher Liang and Jogeshwar Mukherjee
Biomolecules 2025, 15(4), 592; https://doi.org/10.3390/biom15040592 - 16 Apr 2025
Viewed by 161
Abstract
Serotonin 5HT1A receptors may be affected in neurodegeneration, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Using the selective 5HT1A receptor positron emission tomography (PET) imaging agent, [18F]mefway, autoradiographic studies from postmortem human brains of AD, PD, and [...] Read more.
Serotonin 5HT1A receptors may be affected in neurodegeneration, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Using the selective 5HT1A receptor positron emission tomography (PET) imaging agent, [18F]mefway, autoradiographic studies from postmortem human brains of AD, PD, and cognitively normal (CN) subjects were carried out. Levels of [18F]mefway binding were compared with monoamine oxidase A (MAO-A) measured using [18F]FAZIN3 binding and dopamine D2/D3 receptors measured using [18F]fallypride binding in the same subjects. Autoradiograms of brain sections of the anterior cingulate and corpus callosum from CN, PD, and AD subjects (n = 6 in each group) were analyzed. Significant increased binding of [18F]mefway was found in the AD (+30%) and PD (+11%) brains compared to CN brains. This increase positively correlated to increased [18F]FAZIN3 binding, suggesting greater 5HT1A receptor availability when MAO-A levels are higher. Differences in [18F]fallypride binding in the three groups were not significant. Our results support the finding that the availability of 5HT1A receptors in AD and PD is elevated in the anterior cingulate cortex and is negatively correlated with MAO-A. This upregulation may potentially be a response to lower serotonin levels due to the increased levels of MAO-A activity in this brain region or other neuroinflammatory changes. Thus, 5HT1A receptors may be a potential target for diagnostic and therapeutic approaches for AD and PD. Full article
(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration—2nd Edition)
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