|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Cx3cr1-deficiency exacerbates alpha-synuclein-A53T induced neuroinflammation and neurodegeneration in a mouse model of Parkinson's disease.
|
29624735 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Finally, microglial GR sensitivity to A53T-alpha-synuclein induced DN degeneration as well as decreased microglial GR expression observed in SN of PD brain samples, all suggest that reduced microglial GR activity in SN can stimulate TLR9 activation and DN loss in PD pathology.
|
29934589 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
NCX1 and NCX3 as potential factors contributing to neurodegeneration and neuroinflammation in the A53T transgenic mouse model of Parkinson's Disease.
|
29941946 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
A53T-α-synuclein overexpression in murine locus coeruleus induces Parkinson's disease-like pathology in neurons and glia.
|
29747690 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Despite converging epidemiological evidence for the inverse relationship of regular caffeine consumption and risk of developing Parkinson's disease (PD) with animal studies demonstrating protective effect of caffeine in various neurotoxin models of PD, whether caffeine can protect against mutant α-synuclein (α-Syn) A53T-induced neurotoxicity in intact animals has not been examined.
|
29770111 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Proteinaceous depositions of alpha-synuclein (α-syn) and its mutations, A30P and A53T, are one important characteristic of PD.
|
29649746 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Alpha-synuclein A53T transgenic mouse (A53T) is an essential tool to investigate the onsets and the extents of PD non-motor symptoms.
|
29218419 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
The effects of stable overexpression of γ-synuclein (γ-syn), a neuronal protein recently recognized as a novel regulator of lipid handling in adipocytes, and transient overexpression of Parkinson's disease (PD) α-synuclein [α-syn; wild-type (wt) and its pathogenic mutants A53T, A30P and E46K] in SH-SY5Y and T98G cells, were also evaluated.
|
29713567 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
This study demonstrates that reduced GCase activity both in the context of heterozygous GBA1 mutation associated with PD and in old age, contribute to increased aggregation of mutant α-syn A53T and exacerbates the phenotype in a fly model of PD.
|
29503608 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Subjects (rat and NHP) received targeted enteric injections of PFFs or adeno-associated virus overexpressing the Parkinson's disease associated A53T α-syn mutant.
|
29341898 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Erythrocyte membranes were obtained from PD patients (mutation carriers in the α-synuclein gene (A53T-PD) and glucocerebrosidase gene (GBA-PD) (n=18 each), and patients without known mutations (GU-PD, n=56)), and age-/sex-matched controls (n=56).
|
29129675 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Genomic DNA levels of mutant alpha-synuclein correlate with non-motor symptoms in an A53T Parkinson's disease mouse model.
|
29355568 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ten-month-old α-synuclein A53T mice, a model of Parkinson's disease (PD), were treated with chronic restraint stress (CRS) to simulate a PD-sensitive person with constant stress stimulation.
|
29130486 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Collectively, our results are the first to demonstrate a gene by environment interaction in PD, whereby agrochemical exposure selectively triggers a deficit in mitochondrial transport by nitrating the microtubules in neurons harboring the SNCA-A53T mutation.-Stykel, M. G., Humphries, K., Kirby, M. P., Czaniecki, C., Wang, T., Ryan, T., Bamm, V., Ryan, S. D. Nitration of microtubules blocks axonal mitochondrial transport in a human pluripotent stem cell model of Parkinson's disease.
|
29688812 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
We now report on the difference in the breath-print and content of VOCs between rats with mild and severe lesions of DA neurons, serotonergic neuronal lesions, and transgenic (Tg) rats carrying the PD-producing A53T mutation of the SNCA (α-synuclein) gene.
|
29017011 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Eight-month-old transgenic (Tg) PD mice that overexpress human A53T α-synuclein (α-syn) were randomly allocated to an EE or standard conditions for 2 mo.
|
29707965 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Generation of gene-corrected iPSC line from Parkinson's disease patient iPSC line with alpha-SNCA A53T mutation.
|
29906669 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here we first provided evidence that RV treatment alleviated motor and cognitive deficits in the A53T α-synuclein mouse model of PD in a dose-dependent manner.
|
30462117 |
2018 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
In this study, we developed a new PD model in the transgenic mice expressing mutant hemizygous (hemi) or homozygous (homo) A53T α-synuclein (α-syn Tg) and their wildtype (WT) littermates by treatment with sub-toxic (10 mg/kg, i.p., daily for 5 days) or toxic (30 mg/kg, i.p., daily for 5 days) dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
|
29200905 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Using seed growth by monomer association (SeGMA) assays to measure fibril growth over 3 h in the presence of C2-α-syn monomer, we observed that some familial PD-associated α-syn mutations (<i>i.e.</i> H50Q and A53T) greatly increased growth rates, whereas others (E46K, A30P, and G51D) decreased growth rates.
|
28373279 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
A53T mutant α-synuclein-transfected cells (A53T AS cells) plus MPP<sup>+</sup> exposure were used as a complex cell model of PD.
|
28187263 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
We show here that CCT inhibits amyloid fibre assembly of α-synuclein A53T, one of the mutants responsible for Parkinson's disease.
|
28102321 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
We applied STN-DBS in an adeno-associated virus (AAV) 1/2-driven human mutated A53T α-synuclein (aSyn)-overexpressing PD rat model (AAV1/2-A53T-aSyn).
|
28470693 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
A53T) are known to be directly associated with Parkinson's disease (PD).
|
28442946 |
2017 |
|
rs104893877
|
|
Parkinson Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Our results reveal that A53T α-synuclein (oligomers or aggregates) leads to the inhibition of mitochondrial trafficking, which can be rescued by NAP, suggesting the involvement of microtubule disruption in the pathophysiology of Parkinson's disease.
|
27866262 |
2017 |