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Neurology International
Special Issues
Advances in Molecular Mechanisms of Neurodegenerative Diseases
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Advances in Molecular Mechanisms of Neurodegenerative Diseases

A special issue of Neurology International (ISSN 2035-8377). This special issue belongs to the section "Movement Disorders and Neurodegenerative Diseases".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 1200

Special Issue Editors

Dr. Pravin Hivare

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Guest Editor
Department of Neurology, School of Medicine, University of Utah, 20 South 2030 East, Salt Lake City, 84113 UT, USA
Interests: neuroscience; neurodegeneration; endocytic mechanisms; Alzheimer’s disease; Parkinson’s disease; spinocerebellar ataxias type 2 (SCA2); Amyotrophic lateral sclerosis (ALS); RNA sequencing; super-resolution microscopy; protein aggregation; proteomics; rodent models; therapeutic development
Dr. Joshna Gadhavi

E-Mail Website
Guest Editor
Department of Biochemistry, School of Medicine, Emory University, Whitehead Biomedical Research Building, 615 Michael St., Atlanta, GA 30322, USA
Interests: neuroscience; neurodegeneration; Alzheimer’s disease; Parkinson’s disease; amyloid proteins aggregation; prion protein aggregation; neurodegenerative disease; biomarkers development; plasma and CSF biomarkers development; neuronal cell culture development
Dr. Cristoforo Comi

E-Mail Website
Guest Editor
1. Neurology Unit, S. Andrea Hospital, Department of Translational Medicine, University of Piemonte Orientale, Corso Abbiate 21, 13100 Vercelli, Italy
2. Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy
3. Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), University of Piemonte Orientale, 28100 Novara, Italy
Interests: neurodegenerative diseases including Parkinson’s disease; Huntington’s disease; other movement disorders; Alzheimer’s disease; neuroimmune diseases including: multiple sclerosis, inflammatory neuropathies, myasthenia gravis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis, among others, represent a significant and growing public health challenge. Various key factors contribute to the development of these diseases, such as genetic mutations, protein misfolding and aggregation, neuroinflammation, mitochondrial and oxidative pathways, impaired clearance pathways, epigenetic changes, etc. Despite tremendous progress in research, the precise molecular mechanisms driving these diseases remain incompletely understood, hindering the development of effective therapies. This Special Issue, “Advances in Molecular Mechanisms of Neurodegenerative Diseases”, seeks to compile cutting-edge research that elucidates the complex molecular and cellular processes underlying neurodegeneration.

This Special Issue aims to explore the latest research findings and state-of-the-art reviews on various aspects of neurodegenerative diseases, including molecular and cellular mechanisms of amyloid protein aggregation, disease pathology associated with neuroinflammation, mitochondrial abnormalities, oxidative stress, dysfunctions in lysosomal, endocytic, and autophagy-related pathways, and genetic and epigenetic factors to advance our understanding of neurodegeneration and to further facilitate early diagnosis and effective therapeutic development.

Research topics of interest include (but not limited to) the following:

  1. Understanding the molecular and cellular mechanisms of amyloid protein aggregation.
  2. Understanding the molecular and cellular mechanisms for mitochondrial anomalies.
  3. Understanding the autophagy-related dysfunctions in various neurodegenerative diseases.
  4. Identifying novel biomarkers and genetic factors for early diagnosis.
  5. Discovering therapeutic strategies for the prevention and treatment of neurodegenerative diseases.

Dr. Pravin Hivare
Dr. Joshna Gadhavi
Dr. Cristoforo Comi
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Neurology International is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). 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
  • molecular mechanisms
  • protein aggregation
  • endocytic pathways
  • mitochondrial dysfunction
  • oxidative stress
  • neuroinflammation
  • autophagy
  • genetics
  • therapeutic targets
  • biomarker identification

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Published Papers (3 papers)

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Review

15 pages, 1091 KB  
Review
Consensus Molecules Associated with Parkinson’s Disease
by Sara Eyal, Shira Alfasi, Karin Ben Zaken, Ibrahim O. Sawaid, Lior Segev, Samuel Mesfin, Pnina Frankel, Rahaf Ezzy, Trishna Saha-Detroja, Shilpa Madhavan, Naamah Bloch, Baruh Polis and Abraham O. Samson
Neurol. Int. 2026, 18(2), 23; https://doi.org/10.3390/neurolint18020023 - 27 Jan 2026
Viewed by 100
Abstract
Parkinson’s disease (PD) has been associated with some types of food and drugs. Here, we query PubMed for the association of PD with foods and drugs, using a list of 217,776 compounds derived from the Human Metabolome Database (HMDB). To calculate associations, a [...] Read more.
Parkinson’s disease (PD) has been associated with some types of food and drugs. Here, we query PubMed for the association of PD with foods and drugs, using a list of 217,776 compounds derived from the Human Metabolome Database (HMDB). To calculate associations, a Python script was developed to query PubMed for co-citations of PD with each compound, and adjust this count for compound abundance. Notably, PD is found to be associated with small-molecule drugs, adjunctive therapies, contraindicated drugs, diagnostic agents, biomarkers, conditional essential molecules, and inducers. Drugs include L-dopa (49%), carbidopa (63%), benserazide (50%), entacapone (74%), tolcapone (56%), rasagiline (76%), selegiline (46%), pargyline (4%), ropinirole (61%), pramipexole (56%), lisuride (27%), cabergoline (16%), bromocriptine (12%), and zonisamide (9%). Adjunctive therapies include droxidopa (33%), trihexyphenidyl (28%), biperiden (17%), amantadine (24%), memantine (7%), rivastigmine (13%), donepezil (6%), galantamine (4%), domperidone (6%), clonazepam (4%), tetrabenazine (16%), mazindol (13%), quetiapine (6%), and clozapine (4%). Contraindicated drugs include haloperidol (4%), sulpiride (3%), and methyldopa (6%). Diagnostic agents include FP-CIT (60%) and beta-CIT (43%). Biomarkers include 3-methoxytyrosine (48%) and homovanillic acid (12%). Endogenous cofactors include tetrahydrobiopterin (4%) and Coenzyme Q10 (4%). Chemical inducers of PD include 6-hydroxydopamine (40%), N-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 78%), tetrahydropyridine (77%), probenecid (4%), quinolinic acid (4%), 1,2,3,4-tetrahydroisoquinoline (TIQ, 16%), salsolinol (32%), rotenone (25%), and β-Methylamino-L-alanine (BMAA, 29%). Notably, our study highlights conditional essential endogenous cofactors associated with PD and emphasizes rational directions for investigation in PD. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Neurodegenerative Diseases)
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16 pages, 2407 KB  
Review
Modeling Late-Onset Sporadic Alzheimer’s Disease Using Patient-Derived Cells: A Review
by Alisar Katbe, Ismaïla Diagne and Gilbert Bernier
Neurol. Int. 2026, 18(1), 17; https://doi.org/10.3390/neurolint18010017 - 14 Jan 2026
Viewed by 233
Abstract
Late-onset sporadic Alzheimer’s disease (LOAD) is the most common form of dementia. The disease is characterized by progressive loss of memory and behavioral changes followed by neurodegeneration of all cortical areas. While the contribution of genetic and environmental factors is important, advanced aging [...] Read more.
Late-onset sporadic Alzheimer’s disease (LOAD) is the most common form of dementia. The disease is characterized by progressive loss of memory and behavioral changes followed by neurodegeneration of all cortical areas. While the contribution of genetic and environmental factors is important, advanced aging remains the most important disease risk factor. Because LOAD does not naturally occur in most animal species, except humans, studies have traditionally relied on the use of transgenic mouse models recapitulating early-onset familial Alzheimer’s disease (EOAD). Hence, the development of more representative LOAD models through reprograming of patient-derived cells into neuronal, glial, and immune cells became a necessity to better understand the disease’s origin and pathophysiology. Herein, and focusing on neurons, we review current work in the field and compare results obtained with two different reprograming methods to generate LOAD patient’s neuronal cells: the induced pluripotent stem cell and induced neuron technologies. We also evaluate if these models can faithfully mimic cellular and molecular pathologies observed in LOAD patients’ brains. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Neurodegenerative Diseases)
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14 pages, 594 KB  
Review
Experimental Primary Brain Calcification Model and Its Application to Pathogenesis Mechanism Analysis and Therapeutic Research
by Hisaka Kurita, Junya Murata, Kazuki Ohuchi, Yuichi Hayashi and Masatoshi Inden
Neurol. Int. 2026, 18(1), 4; https://doi.org/10.3390/neurolint18010004 - 24 Dec 2025
Viewed by 361
Abstract
Primary Brain Calcification (PBC) is a neurodegenerative disorder of unknown etiology that results in bilateral calcifications within the brain. PBC symptoms vary, including Parkinsonian symptoms and psychiatric symptoms. Abnormalities in phosphate metabolism within the brain are hypothesized to be a mechanism underlying the [...] Read more.
Primary Brain Calcification (PBC) is a neurodegenerative disorder of unknown etiology that results in bilateral calcifications within the brain. PBC symptoms vary, including Parkinsonian symptoms and psychiatric symptoms. Abnormalities in phosphate metabolism within the brain are hypothesized to be a mechanism underlying the onset of PBC, but the precise pathophysiological mechanism remains unclear. Furthermore, no fundamental treatment or therapeutic agent for PBC has been established. Previous studies have reported SLC20A2, PDGFB, PDGFRB, XPR1, MYORG, JAM2, CMPK2, and NAA60 as causative genes for familial PBC. Elucidating the pathophysiological mechanisms of PBC and developing treatments and therapeutic agents requires appropriate experimental disease models. Knockout mice and mutant mice targeting familial causative genes have been reported to be useful as in vivo models of PBC. Furthermore, several disease-specific iPS cells for PBC have been reported, suggesting their potential utility as PBC models. This paper reviews each familial causative gene and current PBC models, including genetically modified animals and disease-specific iPS cells, and examines their usefulness for understanding disease mechanisms and advancing therapeutic research. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Neurodegenerative Diseases)
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