Background: Neurodegenerative genes are critical in neuronal loss in Parkinson's disease (PD). We performed a systematic meta-analysis including all the studies published on PD risk related to genes encoding enzymes vital for dopamine metabolism and neuron survival.
Methods: We included neurodegeneration-related genes which were divided into four groups according to their functions: main enzymes in dopamine metabolism, receptors and transporters for dopamine or other metabolites, neuroprotective factors for dopaminergic neurons, and genes associated with dopaminergic neurons survival reported in other neurological diseases. We collected original articles from PubMed, Embase, and Web of Science databases. Revman 5.3 software was used to analyze data. The allele model (AM) was used to test the effect size of the effect allele between the case group and the control group and secondary analysis using the dominant model (DM) and recessive model (RM) to analyze the contributions from heterozygote and homozygote to the allele risk. Odds ratio (OR) and 95% confidence interval (CI) were used to present the pooled results.
Results: We included 31 variants in 20 genes for the final pooled analysis. Consequently, SLC6A4/5-HTT HTTLPR, BDNF rs56164415, FGF20 rs1721100, PARK16 rs823128, rs823156, rs947211, APOE e2, A2M rs669, RIT2 rs12456492, MAPT intron 9 H1H2, and STH rs62063857 variants were statistically associated with PD risk while researched variants in COMT, DBH, MAO, DAT/SLC6A3, DRD2, GRIN2B, GSK3β, ATP13A2, LINGO1, PICALM, and GRN were not related to PD risk.
Conclusion: Several variants from neurodegeneration-related genes are associated with PD risk, which may help deepen the understanding of PD pathogenesis and improve clinical treatment strategies.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10072-022-06192-8 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mechanisms by which Ganglioside GM1, a specific type of glycosphingolipid, ameliorates BMAA-induced neurotoxicity in early-life stage of zebrafish embryos.
Food Res Int
January 2025
State Key Laboratory of Marine Food Processing & Safety Control, College of Food Science and Engineering, Ocean University of China, Qingdao 266404, China; Qingdao Marine Science and Technology Center, Qingdao, Shandong Province 266235, China.
The neurotoxin β-methylamino-L-alanine (BMAA) produced by cyanobacteria is widely present in foods and dietary supplements, posing a significant threat to human health. Ganglioside GM1 (GM1) has demonstrated potential for treating neurodegenerative diseases; however, its ability to prevent BMAA-induced neurotoxicity remains uncertain. In this study, zebrafish embryos were treated with Ganglioside GM1 to investigate its neuroprotective effects against BMAA exposure and the underlying mechanisms.
View Article and Find Full Text PDFDifferential Expression of Neurodegeneration-Related Genes in SH-SY5Y Neuroblastoma Cells Under the Influence of Cyclophilin A: Could the Enzyme be a Likely Trigger and Therapeutic Target for Alzheimer's Disease?
Neurochem Res
December 2024
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
The function and mechanism of Cyclophilin A (CypA) in modulating gene expression associated with Alzheimer's disease (AD) remain unclear. This multifunctional protein is found to be elevated in the cerebrospinal fluid (CSF) of individuals at risk for AD. The cytotoxic effects of CypA, including both wild-type and the mutant R55A, were assessed using the MTT assay.
View Article and Find Full Text PDFMulti-omic analysis of a mucolipidosis II neuronal cell model uncovers involvement of pathways related to neurodegeneration and drug metabolism.
Mol Genet Metab
November 2024
Greenwood Genetic Center, Greenwood, SC 29646, United States of America. Electronic address:
Defining the molecular consequences of lysosomal dysfunction in neuronal cell types remains an area of investigation that is needed to understand many underappreciated phenotypes associated with lysosomal disorders. Here we characterize GNPTAB-knockout DAOY medulloblastoma cells using different genetic and proteomic approaches, with a focus on how altered gene expression and cell surface abundance of glycoproteins may explain emerging neurological issues in individuals with GNPTAB-related disorders, including mucolipidosis II (ML II) and mucolipidosis IIIα/β (ML IIIα/β). The two knockout clones characterized demonstrated all the biochemical hallmarks of this disease, including loss of intracellular glycosidase activity due to impaired mannose 6-phosphate-dependent lysosomal sorting, lysosomal cholesterol accumulation, and increased markers of autophagic dysfunction.
View Article and Find Full Text PDFPlasma miRNAs across the Alzheimer's disease continuum: Relationship to central biomarkers.
Alzheimers Dement
November 2024
Center for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Introduction: MicroRNAs (miRNAs) play important roles in gene expression regulation and Alzheimer's disease (AD) pathogenesis.
Methods: We investigated the association between baseline plasma miRNAs and central AD biomarkers from the Alzheimer's Disease Neuroimaging Initiative (ADNI; N = 803): amyloid, tau, and neurodegeneration (A/T/N). Differentially expressed miRNAs and their targets were identified, followed by pathway enrichment analysis.
Evolutionary perspectives on mRNA signatures of neurodegeneration-related brain remodelling.
Brain
September 2024
Department of Neurology, Penn Frontotemporal Degeneration Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
This scientific commentary refers to ‘Frontotemporal lobar degeneration targets brain regions linked to expression of recently evolved genes’ by Pasquini (https://doi.org/10.1093/brain/awae205).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!