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Genetic Advances in Neurobiology of Health and 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: 28 February 2026 | Viewed by 694

Special Issue Editors


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Guest Editor
Institute for Fundamental Biomedical Research, Biomedical Sciences Research Centre "Alexander Fleming", 34 Fleming Street, 16672 Vari, Greece
Interests: mechanisms of associative and nonassciative learning and memory; Drosophila and mouse models of intelectual disability; neurological and psychiatric conditions
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute for Fundamental Biomedical Research, Biomedical Sciences Research Centre "Alexander Fleming", 34 Fleming Street, 16672 Vari, Greece
Interests: tao protein; Drosophila model; proteomic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Modern genetic approaches benefit from advances in -omics technologies, which enable comprehensive profiling of neuronal physiology, as well as evaluation the overall impact of mutations underlying neurological disorders, acute insults to neurons, and the consequences of pharmacological treatments. Moreover, genome-wide association studies provide important insights into the genetics of complex psychiatric conditions, such as schizophrenia, autism, and neurodegenerative diseases. Although this wealth of new information is rapidly advancing hypotheses regarding the impact of mutations and potentially disease-linked polymorphisms on the transcriptome, post-transcriptome, proteome, and signaling networks of neurons, methods and experimental systems are needed to cross-validate and expand these findings.

This Special Issue, “Genetic Advances in Neurobiology of Health and Disease”, aims to host contributions featuring novel -omics technological developments, informatics, and artificial intelligence predictions, as well as innovative model systems and approaches for their in vivo validation. We particularly welcome contributions that enhance our understanding of hallmark physiological functions of the nervous system and how these are altered in neurological diseases, with the ultimate goal of paving the way toward rational therapeutic interventions.  

Prof. Dr. Efthimios M. C. Skoulakis
Dr. Katerina Papanikolopoulou
Guest Editors

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Keywords

  • genomics
  • proteins
  • proteomics
  • signaling

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Published Papers (1 paper)

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Research

22 pages, 1526 KB  
Article
Temporal Interactome Mapping of Human Tau in Drosophila Reveals Progressive Mitochondrial Engagement and Porin/VDAC1-Dependent Modulation of Toxicity
by Eleni Tsakiri, Martina Samiotaki, Efthimios M. C. Skoulakis and Katerina Papanikolopoulou
Int. J. Mol. Sci. 2025, 26(19), 9741; https://doi.org/10.3390/ijms26199741 - 7 Oct 2025
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Abstract
Tau protein misfolding and aggregation are central to Tauopathies, yet the temporal dynamics of Tau interactions in vivo remain poorly understood. Here, we applied quantitative proteomics to demonstrate that the interactome of human Tau in adult Drosophila brains changes dynamically over a 12-day [...] Read more.
Tau protein misfolding and aggregation are central to Tauopathies, yet the temporal dynamics of Tau interactions in vivo remain poorly understood. Here, we applied quantitative proteomics to demonstrate that the interactome of human Tau in adult Drosophila brains changes dynamically over a 12-day time course, revealing a progressive shift from early cytosolic and ribosomal associations to late enrichment of mitochondrial and synaptic partners. Notably, the mitochondrial pore protein Porin/VDAC1 was identified as a late-stage interactor and functional analyses demonstrated that Tau overexpression impairs mitochondrial respiration, elevates oxidative damage, and disrupts carbohydrate homeostasis. To validate this temporally specific interaction, Porin was downregulated, resulting in reduced Tau mitochondrial association, phosphorylation and aggregation. Paradoxically, however, Porin attenuation exacerbated Tau-induced toxicity, including shortened lifespan, locomotor deficits, and impaired learning. These findings indicate that while Porin facilitates pathological Tau modifications, it is also essential for neuronal resilience, highlighting a complex role in modulating Tau toxicity. Our study provides a temporal map of Tau-associated proteome changes in vivo and identifies mitochondria as critical mediators of Tau-driven neurodegeneration. Full article
(This article belongs to the Special Issue Genetic Advances in Neurobiology of Health and Disease)
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