ReviewNPJ Parkinson's disease2021
Synucleinopathy-associated pathogenesis in Parkinson's disease and the potential for brain-derived neurotrophic factor.
Review in NPJ Parkinson's disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Efficacy of fecal microbiota transplantation in patients with Parkinson's disease: clinical trial results from a randomized, placebo-controlled design.Gut microbes · 2023Trial
- KLF4 in Parkinson's Disease: Decoding the Molecular Puzzle of Neuroinflammation, Oxidative Stress, and Emerging Therapies.Current medical science · 2026Review
- Integrin α5β1 Activation by PHSRN Peptide Elicits Neuroprotection and Functional Recovery in Parkinson's Disease Mice.Antioxidants (Basel, Switzerland) · 2026Article
- Neurotrophins and Galectin-3: Hidden Keys in Neuroinflammation-A Narrative Review.International journal of molecular sciences · 2026Review
- Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms.Health science reports · 2026Article
- BDNF-amyloid-Frontiers in molecular neuroscience · 2026Review
- Modulation of Behavioral, Biochemical, Immunomodulatory, and Transcriptional Profiles by the StrainInternational journal of molecular sciences · 2025Article
- Genotype-Based Housing as a Potential Confounder in Studies Using Transgenic Mouse Models-Insight from the A53T Mouse Model of Parkinson's Disease.Biomedicines · 2025Article
- OTUD5 Protects Dopaminergic Neurons by Promoting the Degradation of α-Synuclein in Parkinson's Disease Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Toward a biological definition of neuronal and glial synucleinopathies.Nature medicine · 2025Review
- Mitochondrial stress disassembles nuclear architecture through proteolytic activation of PKCδ and Lamin B1 phosphorylation in neuronal cells: implications for pathogenesis of age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2025Article
- Enhancements in Parkinson's Disease Management: Leveraging Levodopa Optimization and Surgical Breakthroughs.Current drug targets · 2025Review
- Unlocking the promise of MANF in diseases: Mechanistic insights and therapeutic potentials.Molecular biology reports · 2024Review
- Harnessing BDNF Signaling to Promote Resilience in Aging.Aging and disease · 2024Review
- BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy.Journal of cellular and molecular medicine · 2024Review
- Transcriptomic profiling of early synucleinopathy in rats induced with preformed fibrils.NPJ Parkinson's disease · 2024Article
- Cancer in pathologically confirmed multiple system atrophy.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Article
- Neurotrophic factor-based pharmacological approaches in neurological disorders.Neural regeneration research · 2023Review
- Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review.IBRO neuroscience reports · 2022Review
- Secretome as neuropathology-targeted intervention of Parkinson's disease.Regenerative therapy · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The lack of disease-modifying treatments for Parkinson's disease (PD) is in part due to an incomplete understanding of the disease's etiology. Alpha-synuclein (α-syn) has become a point of focus in PD due to its connection to both familial and idiopathic cases-specifically its localization to Lewy bodies (LBs), a pathological hallmark of PD. Within this review, we will present a comprehensive overview of the data linking synuclein-associated Lewy pathology with intracellular dysfunction. We first present the alterations in neuronal proteins and transcriptome associated with LBs in postmortem human PD tissue. We next compare these findings to those associated with LB-like inclusions initiated by in vitro exposure to α-syn preformed fibrils (PFFs) and highlight the profound and relatively unique reduction of brain-derived neurotrophic factor (BDNF) in this model. Finally, we discuss the multitude of ways in which BDNF offers the potential to exert disease-modifying effects on the basal ganglia. What remains unknown is the potential for BDNF to mitigate inclusion-associated dysfunction within the context of synucleinopathy. Collectively, this review reiterates the merit of using the PFF model as a tool to understand the physiological changes associated with LBs, while highlighting the neuroprotective potential of harnessing endogenous BDNF.
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.