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Molecular Insights in Neurodegeneration
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Molecular Insights in Neurodegeneration

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: 25 September 2025 | Viewed by 904

Special Issue Editor

Dr. Oscar Arias-Carrión

E-Mail Website
Guest Editor
Experimental Neurology, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Ciudad de México 14389, Mexico
Interests: neurodegenerative diseases; neurodegeneration; neuroimaging; neurobiology and brain physiology; behavioural neuroscience
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases represent a growing burden for global health, marked by complex molecular mechanisms that remain incompletely understood. This Special Issue of the International Journal of Molecular Sciences will focus on uncovering the molecular underpinnings of neurodegeneration, including pathways of protein aggregation, mitochondrial dysfunction, oxidative stress, neuroinflammation, and disrupted neuronal signalling. We invite original research and review articles that offer molecular insights into conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, and related disorders. Studies addressing genetic susceptibility, epigenetic regulation, molecular biomarkers, and novel therapeutic targets are especially encouraged. Interdisciplinary contributions incorporating systems biology, transcriptomics, proteomics, and metabolomics are welcome. This issue aims to enhance our understanding of disease mechanisms and support the development of early diagnostics and effective therapeutic strategies.

Dr. Oscar Arias-Carrion
Guest Editor

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

  • neurodegeneration
  • molecular mechanisms
  • protein aggregation
  • neuroinflammation
  • oxidative stress
  • mitochondrial dysfunction
  • Alzheimer’s disease
  • Parkinson’s disease
  • biomarkers
  • therapeutic targets

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Published Papers (1 paper)

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Review

43 pages, 2656 KiB  
Review
α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges
by Oscar Arias-Carrión, Magdalena Guerra-Crespo, Francisco J. Padilla-Godínez, Luis O. Soto-Rojas and Elías Manjarrez
Int. J. Mol. Sci. 2025, 26(11), 5405; https://doi.org/10.3390/ijms26115405 - 4 Jun 2025
Viewed by 741
Abstract
Parkinson’s disease and related synucleinopathies, including dementia with Lewy bodies and multiple system atrophy, are characterised by the pathological aggregation of the α-synuclein (aSyn) protein in neuronal and glial cells, leading to cellular dysfunction and neurodegeneration. This review synthesizes knowledge of aSyn biology, [...] Read more.
Parkinson’s disease and related synucleinopathies, including dementia with Lewy bodies and multiple system atrophy, are characterised by the pathological aggregation of the α-synuclein (aSyn) protein in neuronal and glial cells, leading to cellular dysfunction and neurodegeneration. This review synthesizes knowledge of aSyn biology, including its structure, aggregation mechanisms, cellular interactions, and systemic influences. We highlight the structural diversity of aSyn aggregates, ranging from oligomers to fibrils, their strain-like properties, and their prion-like propagation. While the role of prion-like mechanisms in disease progression remains a topic of ongoing debate, these processes may contribute to the clinical heterogeneity of synucleinopathies. Dysregulation of protein clearance pathways, including chaperone-mediated autophagy and the ubiquitin–proteasome system, exacerbates aSyn accumulation, while post-translational modifications influence its toxicity and aggregation propensity. Emerging evidence suggests that immune responses and alterations in the gut microbiome are key modulators of aSyn pathology, linking peripheral processes—particularly those of intestinal origin—to central neurodegeneration. Advances in biomarker development, such as cerebrospinal fluid assays, post-translationally modified aSyn, and real-time quaking-induced conversion technology, hold promise for early diagnosis and disease monitoring. Furthermore, positron emission tomography imaging and conformation-specific antibodies offer innovative tools for visualising and targeting aSyn pathology in vivo. Despite significant progress, challenges remain in accurately modelling human synucleinopathies, as existing animal and cellular models capture only specific aspects of the disease. This review underscores the need for more reliable aSyn biomarkers to facilitate the development of effective treatments. Achieving this goal requires an interdisciplinary approach integrating genetic, epigenetic, and environmental insights. Full article
(This article belongs to the Special Issue Molecular Insights in Neurodegeneration)
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