The genetic basis of dementia in Parkinson’s disease

2015 ◽  
pp. 163-176
Author(s):  
Rita Guerreiro ◽  
Andrew Singleton
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Basis

Molecular genetic pathways in Parkinson's disease: a review

2005 ◽  
Vol 109 (4) ◽  
pp. 355-364 ◽  
Author(s):  
Shushant Jain ◽  
Nicholas W. Wood ◽  
Daniel G. Healy
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Basis ◽  
Genetic Factors ◽  
Molecular Genetic ◽  
Mendelian Genetics ◽  
Susceptibility Factors ◽  
Increased Risk ◽  
Major Progress ◽  
Made In

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.

scholarly journals Genetic Basis and Novel Treatment Strategies in Parkinson's Disease – A Review

2021 ◽  
Vol 5 (1) ◽  
pp. 1-5
Author(s):  
Nagare Santosh Gangadhar ◽  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Metal Ion ◽  
Genetic Basis ◽  
Neurodegenerative Disorder ◽  
Symptomatic Relief ◽  
Ion Homeostasis ◽  
Treatment Strategies ◽  
Metal Ion Homeostasis ◽  
Disease Modifying

Parkinson's disease (PD) is the 2nd most common progressive neurodegenerative disorder after Alzheimer's disease. Approximately 60000 are diagnosed with Parkinson's disease each year and more than 10 million people are living with PD. PD is a neurodegenerative disorder in addition to the causes of PD are so many, it's not caused by a single pathophysiologic disturbance. So many drugs are available to treat PD but all are only for symptomatic relief no one drug is a disease-modifying agent. Although so many targets are available for targeting the Synuclein alpha, mitochondrial oxidative stress, autophagy, targeting glial cell inflammation, targeting metal ion homeostasis. But till now no one drug is successful in targeting these targets. In this review, we have summarized the genetic basis and novel targets available for the disease-modifying strategy for PD.

scholarly journals A genetic basis for the variable effect of smoking/nicotine on Parkinson’s disease

2012 ◽  
Vol 13 (6) ◽  
pp. 530-537 ◽  
Author(s):  
E M Hill-Burns ◽  
N Singh ◽  
P Ganguly ◽  
T H Hamza ◽  
J Montimurro ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Basis ◽  
Variable Effect

Genetic basis of Parkinson's disease: a brief review

2021 ◽  
pp. 1
Author(s):  
Anas Aljohani ◽  
Alhassan Ahmed ◽  
AbdulBaqi Bukhary ◽  
Syed Nazar
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Basis

scholarly journals Association of a Common Genetic Variant with Parkinson’s Disease is Propagated through Microglia

2021 ◽  
Author(s):  
R. G. Langston ◽  
A. Beilina ◽  
X. Reed ◽  
A. B. Singleton ◽  
C. Blauwendraat ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Basis ◽  
Genetic Variant ◽  
Induced Pluripotent Stem Cell ◽  
Cell Type ◽  
Common Genetic Variant ◽  
Human Frontal Cortex ◽  
Induced Pluripotent

AbstractStudies of the genetic basis of Parkinson’s disease (PD) have identified many disease-associated genetic variants, but the mechanisms linking variants to pathogenicity are largely unknown. PD risk is attributed to both coding mutations in the Leucine-rich repeat kinase 2 (LRRK2) gene and to common non-coding variation upstream of the LRRK2 locus. Here we show that the influence of genotype at non-coding variant rs76904798 on LRRK2 expression is propagated specifically through microglia, in contrast to evaluations based on general rather than genotype-dependent expression. We find evidence of microglia-specific regulatory regions that may modulate LRRK2 expression using single nuclei sequencing analyses of human frontal cortex and confirm these results in a human induced pluripotent stem cell-derived microglia model. Our study demonstrates that cell type is an important consideration in interrogation of the role of non-coding variation in disease pathogenesis.

scholarly journals Festination Correlates with SNCA Polymorphism in Chinese Patients with Parkinson’s Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Jinhua Zheng ◽  
Xinglong Yang ◽  
Quanzhen Zhao ◽  
Sijia Tian ◽  
Hongyan Huang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Logistic Regression ◽  
Genetic Basis ◽  
Univariate Analysis ◽  
Alpha Synuclein ◽  
Chinese Patients ◽  
Motor Symptom ◽  
Consecutive Series ◽  
Snca Gene

The genetic basis of festination, a common motor symptom in Parkinson’s disease (PD), remains unclear. Since polymorphism in the alpha-synuclein (SNCA) gene is associated with PD phenotype, we examined whether such polymorphism is also associated with festination. SNCA polymorphisms rs11931074 and rs894278 were genotyped in a consecutive series of 258 patients with PD, of whom 122 (47.3%) suffered festination. Univariate analysis revealed significant differences in genotype and minor allele frequencies at rs11931074 or rs894278 between patients with festination and those without it (all p<0.05). Based on logistic regression, a GG or GT genotype at rs11931074 was associated with higher risk of festination among patients with PD (OR 2.077, 95% CI 1.111–3.883, p=0.022), as was the TT genotype at rs894278 (OR 2.271, 95% CI 1.246–4.139, p=0.007). Therefore, we conclude that festination is associated with polymorphism at rs11931074 or rs894278 among patients with PD.

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