scholarly journals Editorial: (Thematic Issue Genetic Factors in Parkinson’s Disease)

2014 ◽  
Vol 14 (8) ◽  
pp. 485-485 ◽  
Author(s):  
Jolanta Dorszewska
2021 ◽  
Vol 10 (3) ◽  
pp. 343-357
Author(s):  
Asunur ADALI ◽  
Selinay Başak - ERDEMLİ-KÖSE ◽  
Anıl YİRÜN ◽  
Pınar ERKEKOĞLU

2005 ◽  
Vol 109 (4) ◽  
pp. 355-364 ◽  
Author(s):  
Shushant Jain ◽  
Nicholas W. Wood ◽  
Daniel G. Healy

Major progress has been made in the last decade in understanding the genetic basis of PD (Parkinson's disease) with five genes unequivocally associated with disease. As a result, multiple pathways have been implicated in the pathogenesis of PD, including proteasome impairment and mitochondrial dysfunction. Although Mendelian genetics has been successful in establishing a genetic predisposition for familial PD, this has not been reiterated in the sporadic form. In fact no genetic factors have been unequivocally associated with increased risk for sporadic PD. The difficulty in identifying susceptibility factors in PD has not only been because of numerous underpowered studies, but we have been unable to dissect out the genetic component in a multifactorial disease. This review aims to summarize the genetic findings within PD.


2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Yuan Zhang ◽  
Qiying Sun ◽  
Minhan Yi ◽  
Xun Zhou ◽  
Jifeng Guo ◽  
...  

Although the etiology of Parkinson’s disease (PD) remains unclear, there is increasing evidence of genetic factors contributing to the onset of PD. Various mutations and risk variants of the gene LRRK2 have been reported, but the association between LRRK2 R1628P and PD is still inconsistent. Thus, we conducted a meta-analysis to determine the potential relationship between R1628P and PD. Our study sample was an aggregate of 17 publications, which in total consisted of 9,275 PD patients and 8,114 controls. All of these articles are of high quality according to NOS, and there was no obvious reporting bias or heterogeneity. In a general Asian population, the pooled OR of the risk genotype contrasts was 1.83 (95% CI: 1.57, 2.13). When stratified by ethnicity, the pooled ORs were 1.84 (95% CI: 1.56, 2.18) in a Chinese population and 1.79 (95% CI: 1.27, 2.52) in a non-Chinese population. Our study suggests that LRRK2 R1628P appears to be a risk factor for PD in Asian populations, both Chinese and non-Chinese.


2017 ◽  
Vol 32 (4) ◽  
Author(s):  
Natalia Palacios

AbstractParkinson’s disease (PD) is a neurodegenerative disease of unknown etiology that is thought to be caused by a complex combination of environmental and/or genetic factors. Air pollution exposure is linked to numerous adverse effects on human health, including brain inflammation and oxidative stress, processes that are believed to contribute to the development and progression of PD. This review provides an overview of recent advances in the epidemiology of air pollution and PD, including evidence of the effects of various pollutants (ozone, PM


2018 ◽  
Vol 6 (4) ◽  
pp. 174-181
Author(s):  
Małgorzata Popis

AbstractParkinson's disease is the second most common neurodegenerative disease, affecting about 0,15-0,3% of the world's population. Its characteristic feature is a loss of dopaminergic neurons in the substantia nigra. PD leads to dopamine deficiency and formation of intracellular inclusions called Lewy bodies, whose main ingredient is α-synuclein. Other types of nervous system cells are also affected by changes associated with that disease. The underlying molecular pathogenesis involves multiple pathways and mechanisms: mitochondrial function, oxidative stress, genetic factors, α-synuclein proteostasis, mitochondrial dynamic impairment, and disorders of the mitophagy process. This review summarizes the factors affecting the functioning of the mitochondria and their connection to the development of Parkinson's disease.


2004 ◽  
Vol 23 (1-2) ◽  
pp. 13-22 ◽  
Author(s):  
Daniel Kam Yin Chan ◽  
Dennis Cordato ◽  
Triet Bui ◽  
George Mellick ◽  
Jean Woo

Toxicology ◽  
2013 ◽  
Vol 307 ◽  
pp. 17-23 ◽  
Author(s):  
Efthimios Dardiotis ◽  
Georgia Xiromerisiou ◽  
Christos Hadjichristodoulou ◽  
Aristidis M. Tsatsakis ◽  
Martin F. Wilks ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinran Cui ◽  
Chen Xu ◽  
Liyuan Zhang ◽  
Yadong Wang

Parkinson’s disease (PD) is the second most frequent neurogenic disease after Alzheimer’s disease. The clinical manifestations include mostly motor disorders, such as bradykinesia, myotonia, and static tremors. Since the cause of this pathological features remain unclear, there is currently no radical treatment for PD. Environmental and genetic factors are thought to contribute to the pathology of PD. To identify the genetic factors, some studies employed the Genome-Wide Association Studies (GWAS) method and detected certain genes closely related to PD. However, the functions of these gene mutants in the development of PD are unknown. Combining GWAS and expression Quantitative Trait Loci (eQTL) analysis, the biological meaning of mutation could be explained to some extent. Therefore, the present investigation used Summary data-based Mendelian Randomization (SMR) analysis to integrate of two PD GWAS datasets and four eQTL datasets with the objective of identifying casual genes. Using this strategy, we found six Single Nucleotide Polymorphism (SNP) loci which could cause the development of PD through altering the susceptibility gene expression, and three risk genes: Synuclein Alpha (SNCA), Mitochondrial Poly(A) Polymerase (MTPAP), and RP11-305E6.4. We proved the accuracy of results through case studies and inferred the functions of these genes in PD. Overall, this study provides insights into the genetic mechanism behind PD, which is crucial for the study of the development of this disease and its diagnosis and treatment.


Sign in / Sign up

Export Citation Format

Share Document