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Special Issue "Drosophila Models for Neurodegenerative Diseases: Achievements and Prospects"

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: 31 August 2021.

Special Issue Editors

Dr. Serge Birman
E-Mail Website
Guest Editor
Brain Plasticity Unit, CNRS, ESPCI Paris, PSL Research University, Paris, France
Interests: neurotransmission; behavior; neurological disorders
Dr. Emi Nagoshi
E-Mail Website
Guest Editor
Department of Genetics and Evolution, University of Geneva, Switzerland
Interests: circadian rhythms; sleep; neurodegeneration
Dr. Frank Hirth
E-Mail Website
Guest Editor
King’s College London; Institute of Psychiatry, Psychology and Neuroscience, London, UK; Maurice Wohl Clinical Neuroscience Institute
Interests: brain development and evolution; neuroscience; mental health disorders

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases affect an ever-increasing aging population. The disorders range from motor dysfunction to psychiatric troubles and dementia. So far, no cure is available, but steady progress is being made. Part of this progress is due to studies in the fruit fly Drosophila which have led to major insights into the cellular and molecular mechanisms underlying neurodegeneration.

More than 20 years after the first reports describing neurodegeneration in flies, this IJMS Special Issue aims to summarize what Drosophila studies have contributed to the understanding and treatment of neurodegeneration and what prospects fly models can offer in the future. Given that cures are still unavailable, progress in this field requires a deeper knowledge of the mechanisms underlying brain development, homeostasis, and maintenance, as well as the function of genes, whose mutations are associated with neurodegenerative disorders. This is where recent progress in Drosophila neurodegeneration research could definitively help, as evidenced by various experts in the field whose contribution will be collected in this Special Issue.

Here, we aim to shed light on the benefits of using Drosophila to complement, or even overcome the limitations of studies carried out in humans and other animal models. The advantages of Drosophila are primarily the ease with which it is possible to perform in vivo studies that cover all aspects of the diseases from genes to circuits and behavior; the well-described anatomy and cellular organization of its brain, which is now close to being completely described at the level of neural circuits and synaptic connections; and the dazzling variety of genetic tools that are continuously developed and improved to study gene functions and neuronal activity in situ at cell and circuit resolution.

These ongoing methodological refinements promise to enable us to elucidate every step of the pathogenic processes underlying neurodegeneration, with the ultimate goal to uncover the original causative failures and to test novel targets and treatments to stop or even reverse the progression of these devastating illnesses.

Dr. Serge Birman
Dr. Emi Nagoshi
Dr. Frank Hirth
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 papers will be 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.


  • neurodegeneration
  • Drosophila
  • Alzheimer’s disease
  • Parkinson’s disease
  • motor neuron disease
  • Huntington’s disease
  • dementia
  • repeat expansion disease
  • α-synuclein
  • amyloid beta
  • Tau
  • TDP-43

Published Papers (1 paper)

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Open AccessArticle
Genetic Screen in Adult Drosophila Reveals That dCBP Depletion in Glial Cells Mitigates Huntington Disease Pathology through a Foxo-Dependent Pathway
Int. J. Mol. Sci. 2021, 22(8), 3884; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083884 - 09 Apr 2021
Viewed by 241
Huntington’s disease (HD) is a progressive and fatal autosomal dominant neurodegenerative disease caused by a CAG repeat expansion in the first exon of the huntingtin gene (HTT). In spite of considerable efforts, there is currently no treatment to stop or delay [...] Read more.
Huntington’s disease (HD) is a progressive and fatal autosomal dominant neurodegenerative disease caused by a CAG repeat expansion in the first exon of the huntingtin gene (HTT). In spite of considerable efforts, there is currently no treatment to stop or delay the disease. Although HTT is expressed ubiquitously, most of our knowledge has been obtained on neurons. More recently, the impact of mutant huntingtin (mHTT) on other cell types, including glial cells, has received growing interest. It is currently unclear whether new pathological pathways could be identified in these cells compared to neurons. To address this question, we performed an in vivo screen for modifiers of mutant huntingtin (HTT-548-128Q) induced pathology in Drosophila adult glial cells and identified several putative therapeutic targets. Among them, we discovered that partial nej/dCBP depletion in these cells was protective, as revealed by strongly increased lifespan and restored locomotor activity. Thus, dCBP promotes the HD pathology in glial cells, in contrast to previous opposite findings in neurons. Further investigations implicated the transcriptional activator Foxo as a critical downstream player in this glial protective pathway. Our data suggest that combinatorial approaches combined to specific tissue targeting may be required to uncover efficient therapies in HD. Full article
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