ArticleCurrent genomics2013
Genetic insights into sporadic Parkinson's disease pathogenesis.
Article in Current genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Association between ubiquitin carboxy-terminal hydrolase-L1 S18Y variant and risk of Parkinson's disease: the impact of ethnicity and onset age.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015Pooled it
- Parkinson Disease Pathogenic Variants: Cross-Ancestry Analysis and Microarray Data Validation.Neurology. Genetics · 2026Article
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Stratified signaling network remodeling of kinase-transcription factors' interactions in Parkinson's disease.Bioinformatics advances · 2026Article
- Review
- Neuroinflammatory Mechanisms and Vocalization Biomarkers in theMedical research archives · 2025Article
- HDAC3 Serine 424 Phospho-mimic and Phospho-null Mutants Bidirectionally Modulate Long-Term Memory Formation and Synaptic Plasticity in the Adult and Aging Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Repurposing the memory-promoting meclofenoxate hydrochloride as a treatment for Parkinson's disease through integrative multi-omics analysis.NPJ Parkinson's disease · 2025Article
- Clearance Pathways for α-Synuclein in Parkinson's Disease.Journal of neurochemistry · 2025Review
- Exploring α-Syn's Functions Through Ablation Models: Physiological and Pathological Implications.Cellular and molecular neurobiology · 2025Review
- Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.International journal of molecular sciences · 2025Review
- Review
- Drosophila as an Animal Model To Determine the Functional and Behavioral Significance of Dopamine Transporter Genetic Variations Associated with Brain Disorders.Advances in neurobiology · 2025Review
- CRISPR-Cas technologies in neurodegenerative disorders: mechanistic insights, therapeutic potential, and translational challenges.Frontiers in neurology · 2025Review
- Case Report: A Case of a Patient with Smith-Magenis Syndrome and Early-Onset Parkinson's Disease.International journal of molecular sciences · 2024Article
- The Effect of Neuronal CoQInternational journal of molecular sciences · 2024Article
- Interplay between α-synuclein and parkin genes: Insights of Parkinson's disease.Molecular biology reports · 2024Review
- Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1BMC neuroscience · 2024Article
- Histone post-translational modification and heterochromatin alterations in neurodegeneration: revealing novel disease pathways and potential therapeutics.Frontiers in molecular neuroscience · 2024Review
- CRISPR/Cas9 Gene Editing: A Novel Approach Towards Alzheimer's Disease Treatment.CNS & neurological disorders drug targets · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intensive research over the last 15 years has led to the identification of several autosomal recessive and dominant genes that cause familial Parkinson's disease (PD). Importantly, the functional characterization of these genes has shed considerable insights into the molecular mechanisms underlying the etiology and pathogenesis of PD. Collectively; these studies implicate aberrant protein and mitochondrial homeostasis as key contributors to the development of PD, with oxidative stress likely acting as an important nexus between the two pathogenic events. Interestingly, recent genome-wide association studies (GWAS) have revealed variations in at least two of the identified familial PD genes (i.e. α-synuclein and LRRK2) as significant risk factors for the development of sporadic PD. At the same time, the studies also uncovered variability in novel alleles that is associated with increased risk for the disease. Additionally, in-silico meta-analyses of GWAS data have allowed major steps into the investigation of the roles of gene-gene and gene-environment interactions in sporadic PD. The emergent picture from the progress made thus far is that the etiology of sporadic PD is multi-factorial and presumably involves a complex interplay between a multitude of gene networks and the environment. Nonetheless, the biochemical pathways underlying familial and sporadic forms of PD are likely to be shared.
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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 Socratic graph.