ijms-logo

Journal Browser

Journal Browser

Molecular Targets and Toxic Interactomes of Pathogenic Proteins in Neurodegeneration

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 August 2026) | Viewed by 1957

Editors


E-Mail Website
Guest Editor
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aramaki-Aoba, Aoba-ku, Sendai 980-8578, Japan
Interests: CaM kinase II; neuronal plasticity; neuronal death
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Biomedical Sciences, Fukushima Medical University, Fukushima, Japan
Interests: tyrosine hydroxylase; dopaminergic system; mitochondria; proteasome; α-synuclein; Parkinson’s disease

Special Issue Information

Dear Colleagues,

Neurotoxic mechanisms of causative proteins in neurodegenerative diseases—such as tau protein, TDP-43 and α-synuclein have been linked to cellular processes including endoplasmic reticulum stress, mitochondrial toxicity and dysregulated liquid–liquid phase separation. However, the ultimate molecular targets with which these pathogenic proteins interact, as well as the precise molecular mechanisms underlying their toxicity, remain largely unclear. Moreover, these disease-associated proteins can interact with one another, giving rise to complex and overlapping pathological states. Importantly, the minimal interaction units that are essential for the manifestation of neurotoxicity have yet to be defined. This Special Issue seeks to solicit innovative and groundbreaking studies aimed at identifying interacting molecules at key cellular targets, including endoplasmic reticulum membrane proteins, mitochondrial inner membrane complexes, nuclear RNA-binding factors, the translational machinery and the proteasome. In addition, manuscripts addressing drug discovery challenges that target these molecules are also welcome. We anticipate that this collection will feature transformative research that accelerates the development of causative therapies for neurodegenerative diseases.

Prof. Dr. Kohji Fukunaga
Dr. Ichiro Kawahata
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • neurodegenerative diseases
  • tau protein
  • TDP-43
  • α-synuclein
  • endoplasmic reticulum stress
  • mitochondrial toxicity
  • liquid–liquid phase separation
  • toxic Interactomes

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

21 pages, 13573 KB  
Article
Caveolin-1 Attenuates Excitotoxic Signaling by Regulating NMDA, AMPA, and Kainate Receptor-Mediated Calcium Influx in Hippocampal Neuronal Cultures
by Swapna Kannothum Kandy, Madhura Milind Nimonkar, Suravi Sasmita Dash, Prashanth N. Vashista, Bhupesh Mehta and Yogananda S. Markandeya
Int. J. Mol. Sci. 2026, 27(12), 5637; https://doi.org/10.3390/ijms27125637 - 22 Jun 2026
Viewed by 1638
Abstract
Glutamate excitotoxicity is a critical pathological mechanism underlying neuronal death in ischemic stroke, epilepsy, and neurodegenerative diseases. Caveolin-1 (Cav-1), a structural protein of caveolae membrane microdomains, has emerged as a potential modulator of neuronal survival, yet its precise mechanisms in excitotoxicity remain incompletely [...] Read more.
Glutamate excitotoxicity is a critical pathological mechanism underlying neuronal death in ischemic stroke, epilepsy, and neurodegenerative diseases. Caveolin-1 (Cav-1), a structural protein of caveolae membrane microdomains, has emerged as a potential modulator of neuronal survival, yet its precise mechanisms in excitotoxicity remain incompletely understood. In this study, we investigated the role of Cav-1 in regulating glutamate-induced calcium dysregulation, reactive oxygen species (ROS) generation, and mitochondrial dysfunction in primary hippocampal neurons. Using Cav-1 overexpression (Cav-1OE) and Cav-1 knockdown (Cav-1KD) approaches, we demonstrate that Cav-1OE significantly attenuates glutamate-stimulated intracellular Ca2+ elevation, reduces ROS generation, and prevents mitochondrial membrane potential (Ψm) depolarization. Further investigation revealed that Cav-1OE reduces, while Cav-1KD enhances, calcium responses mediated by NMDA, AMPA, and KA receptors. These findings establish that Cav-1 functionally attenuates excitotoxic signaling by negatively regulating ionotropic glutamate receptor-mediated Ca2+ influx. Full article
Show Figures

Graphical abstract

Back to TopTop