|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Cortical overexpression of human α-synuclein is not sufficient to produce cognitive dysfunction, whereas combining this overexpression with fibril seeds yields both cognitive and histopathological phenotypes that are relevant to human Lewy body disease.
|
31449702 |
2019 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of this study was to reveal the relationship between misfolded α-Syn aggregate concentration in cerebrospinal fluid (CSF) and cognitive decline risk in PD.
|
30346044 |
2019 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, our data suggest that plasma pS129-α-synuclein levels correlate with motor severity and progression, but not cognitive decline, in patients with PD.
|
31623323 |
2019 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, the role of physiological α-synuclein in cognitive impairment remains undetermined.
|
30958793 |
2019 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Lewy bodies inclusion and aggregation of α-Synuclein (α-Syn) during the pathogenesis of Parkinson's disease (PD) serve as a good example and are potentially linked to other pathological PD features such as progressive dopaminergic neuron cell death, behavioral defects, and nonmotor symptoms like anosmia, cognitive impairment, and depression.
|
30482039 |
2019 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Significantly, removal of endogenous mouse tau expression in TgA53T mice (TgA53T/mTau<sup>-/-</sup>), achieved by mating TgA53T mice to mouse tau-knockout mice, completely ameliorates cognitive dysfunction and concurrent synaptic deficits without affecting αS expression or accumulation of selected toxic αS oligomers.
|
31168644 |
2019 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Lower values in the mismatch between α-synuclein and p-tau181 predicted faster cognitive decline (β= 0.64, p = 0.0012, 95% CI [(0.48)-(0.84)]).
|
29376878 |
2018 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CSF total α-synuclein levels did not distinguish PD patients from controls, displayed no substantial changes during a period of up to 4 years, and did not predict subsequent motor or cognitive decline.
|
29409704 |
2018 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
We focus primarily on the prion protein and propose a pathological mechanism in which the interaction between α-synuclein and prion protein leads to the formation of cofilin/actin rods, culminating in long-term potentiation impairment and cognitive dysfunction.
|
30423195 |
2018 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results suggest that, though underlying mechanisms remain to be defined, alterations in plasma total and NDE α-synuclein concentrations are likely associated with PD progression, especially in the aspect of cognitive impairment, at early stages of the disease.
|
29705185 |
2018 |
|
Impaired cognition
|
0.100 |
GeneticVariation
|
disease |
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 |
|
Impaired cognition
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, we aimed to explore the longitudinal changes of CSF a lpha-synuclein (α-syn), total tau (t-tau), phosphorylated tau (p-tau), and beta-amyloid (Aβ<sub>1-42</sub>) and their relationships with each other and with baseline clinical entities like REM sleep behavior disorder (RBD), cognitive impairment, motor symptoms, and olfaction dysfunction.
|
30050494 |
2018 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The presence of RBD was a predictor for motor progression only in patients with PD who had both low α-synuclein levels and low [<sup>123</sup>I]FP-CIT uptake in the striatum (HR = 2.091, 95% CI = 1.116-3.918; <i>p</i> = 0.021) and a predictor for cognitive decline only in patients with PD who had both low Aβ<sub>42</sub> and low α-synuclein levels (HR = 2.810, 95% CI = 1.462-5.400; <i>p</i> = 0.002).
|
30089615 |
2018 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
At the same time that the alpha-synuclein era was developing, clinical advances took place by recognizing PD as hosting a wide variety of nonmotor features with eventual cognitive impairment in many.Therapeutics has also evolved.
|
28784297 |
2018 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Longitudinal studies indicate that low levels of CSF Aβ42 are predictive of cognitive decline; however, results for tau and α-Syn were not consistent.
|
28554411 |
2017 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Indeed, comp-B reduces not only α-synuclein but also insoluble Aβ42 levels, prevents the reductions in synaptophysin and drebrin, and rescues cognitive deficits in transgenic APdE9 mice model of AD.
|
27802241 |
2017 |
|
Impaired cognition
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Hence, alpha-synuclein p.A53V homozygous mutation leads to a distinct phenotype of progressive parkinsonism and cognitive decline, commonly observed in patients with SNCA missense mutation or multiplications.
|
28666710 |
2017 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Objectives:</b> To determine the prevalence of cognitive impairment in patients with PD using Montreal Cognitive Assessment (MoCA), Comprehensive Trail Making Test (CTMT) and Parkinson's disease-cognitive rating scale (PDCRS), and its association with plasma α-synuclein and <i>ApoE</i> genetic polymorphisms.
|
29326545 |
2017 |
|
Impaired cognition
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Importantly, the abundance of αSyn oligomers in human brain tissue correlated with cognitive impairment and reductions in synapsin expression.
|
28533388 |
2017 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
α-synuclein interacts with PrP<sup>C</sup> to induce cognitive impairment through mGluR5 and NMDAR2B.
|
28945221 |
2017 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Plasma α-synuclein could serve as a surrogate biomarker for patients at risk of cognitive decline.
|
28550072 |
2017 |
|
Impaired cognition
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We found that over half of the reported cases with SNCA duplication had early-onset parkinsonism and non-motor features, such as dysautonomia, rapid eye movement sleep behavior disorder (RBD), hallucinations (usually visual) and cognitive deficits leading to dementia.
|
26350119 |
2016 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Abnormal α-synuclein (α-syn) accumulation in the CNS may underlie neuronal cell and synaptic dysfunction leading to motor and cognitive deficits in synucleinopathies including Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB).
|
27389831 |
2016 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study reveals a consistent association of reduced SNCA transcripts in accessible peripheral blood and early-stage Parkinson's disease in 863 participants and suggests a clinical role as potential predictor of cognitive decline.
|
26220939 |
2015 |
|
Impaired cognition
|
0.100 |
Biomarker
|
disease |
BEFREE |
Role of α-synuclein in cognitive dysfunction: Studies in Drosophila melanogaster.
|
25954925 |
2015 |