ReviewNPJ Parkinson's disease2022
Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson's disease.
Review in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Simultaneous Whole-Cell Recording and Calcium Imaging Does Not Reveal Electrically Coupled Neurons ineNeuro · 2026Article
- Association Between Blood-Brain Barrier Disruption and Gut Microbiota Dysbiosis in Parkinson's Disease.Cellular and molecular neurobiology · 2026Review
- Diverse roles of connexins in the neuro-vasculature in homeostasis and disease.Translational neuroscience · 2026Review
- Alpha-synuclein overexpression reduces neural activity within a basal ganglia vocal nucleus in a zebra finch model.PloS one · 2026Article
- Composite Behavior of Nanopore Array Large Memristors.Micromachines · 2025Article
- Recent advances in targeting LRRK2 for Parkinson's disease treatment.Journal of translational medicine · 2025Review
- Identification and Validation of Biomarkers for Alzheimer's Disease Based on Akt and Wnt Signaling Pathways in Mouse Models.Molecular neurobiology · 2025Article
- Article
- Participation of Lens Proteins and miRs in Traumatic and Inheritance Cataract: A Review on Diagnostic and Therapeutic Approaches for Cataract Management.Current pharmaceutical biotechnology · 2025Review
- Alpha-synuclein null mutation exacerbates the phenotype of a model of Menkes disease in female mice.Frontiers in neuroscience · 2025Article
- Microbiota-Gut-Brain Axis in Age-Related Neurodegenerative Diseases.Current neuropharmacology · 2025Review
- Robust In Vitro Models for Studying Parkinson's Disease? LUHMES Cells and SH-SH5Y Cells.International journal of molecular sciences · 2024Article
- Brain-Region-Specific Differences in Protein Citrullination/Deimination in a Pre-Motor Parkinson's Disease Rat Model.International journal of molecular sciences · 2024Article
- Microarray-based Analysis of Differential Gene Expression Profile in Rotenone-induced Parkinson's Disease Zebrafish Model.CNS & neurological disorders drug targets · 2024Article
- Gut microbiota defined epigenomes of Alzheimer's and Parkinson's diseases reveal novel targets for therapy.Epigenomics · 2024Review
- Whole Transcriptome Analysis of Substantia Nigra in Mice with MPTP-Induced Parkinsonism Bearing Defective Glucocerebrosidase Activity.International journal of molecular sciences · 2023Article
- Role of Exosomes in the Pathogenesis and Theranostic of Alzheimer's Disease and Parkinson's Disease.International journal of molecular sciences · 2023Review
- Outlook of PINK1/Parkin signaling in molecular etiology of Parkinson's disease, with insights intoZoological research · 2023Review
- Neurotransmitters in Type 2 Diabetes and the Control of Systemic and Central Energy Balance.Metabolites · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurological disorder that affects the movement of the human body. It is primarily characterized by reduced dopamine levels in the brain. The causative agent of PD is still unclear but it is generally accepted that α-synuclein has a central role to play. It is also known that gap-junctions and associated connexins are complicated structures that play critical roles in nervous system signaling and associated misfunctioning. Thus, our current article emphasizes how, alongside α-synuclein, ion-channels, gap-junctions, and related connexins, all play vital roles in influencing multiple metabolic activities of the brain during PD. It also highlights that ion-channel and gap-junction disruptions, which are primarily mediated by their structural-functional changes and alterations, have a role in PD. Furthermore, we discussed available drugs and advanced therapeutic interventions that target Parkinson's pathogenesis. In conclusion, it warrants creating better treatments for PD patients. Although, dopaminergic replenishment therapy is useful in treating neurological problems, such therapies are, however, unable to control the degeneration that underpins the disease, thereby declining their overall efficacy. This creates an additional challenge and an untapped scope for neurologists to adopt treatments for PD by targeting the ion-channels and gap-junctions, which is well-reviewed in the present article.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.