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Mechanisms research papers
Protection of MPTP-induced neuroinflammation and neurodegeneration by rotigotine-loaded microspheres
These results suggest that CDS therapy can play a neuroprotective role in an MPTP mouse model. Neuroprotective disease-modifying therapy may have the potential benefits of early treatment by normalizing compensatory mechanisms and may also help to delay dyskinesia in the later stages of PD.
30 January 2015
The MC1R melanoma risk variant p.R160W is associated with Parkinson's disease
Authors found that the MC1R variant p.R160W (rs1805008) is marginally associated with Parkinson's disease (OR=2.10; gender- and age-adjusted P=0.009; Bonferroni-corrected P=0.063). Our results suggest that MC1R genetic variants modulate the risk of Parkinson's disease in the Spanish population.
29 January 2015
Quantitative Expression Proteomics and Phosphoproteomics Profile of Brain from PINK1 Knockout Mice: Insights into Mechanisms of
The observed changes in the brain proteome and phosphoproteome of mice lacking PINK1 suggest that defects in signaling networks, energy metabolism, cellular proteostasis and neuronal structure and plasticity are involved in the pathogenesis of familial PD.
27 January 2015
Statins, plasma cholesterol, and risk of Parkinson's disease: A prospective study
Statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk. These data are inconsistent with the hypothesis that statins are protective against PD.
14 January 2015
Beneficial effects of nicotine, cotinine and its metabolites as potential agents for Parkinson's disease
The effect of nicotine and some of its derivatives on dopaminergic neurons viability, neuroinflammation, and motor and memory functions, have been investigated using cellular and rodent models of PD. Current evidence shows that nicotine, and some of its derivatives diminish oxidative stress and neuroinflammation in the brain and improve synaptic plasticity and neuronal survival of dopaminergic neurons.
09 January 2015
Network-based metaanalysis identifies HNF4A and PTBP1 as longitudinally dynamic biomarkers for Parkinson's disease
Study data suggest that knocking down LRRK2 may protect from overt cell loss by inhibiting the recruitment of chronically activated proinflammatory myeloid cells. These results may provide value in the translation of LRRK2-targeting therapeutics to conditions where neuroinflammation may underlie aspects of neuronal dysfunction and degeneration.
07 January 2015
miRNA expression is highly sensitive to a drug therapy in Parkinson's disease
Conclusions: It is probable that miRNAs are very sensitive to drug therapy and that the effects of therapy observed may be associated with changes in the levels of these miRNAs and their target genes in patients with Parkinson's disease.
01 January 2015
Assessing the Utility of the MDS Task Force Level 1 Diagnostic Criteria for Mild Cognitive Impairment in P
Results from the present study suggest that the MDS PD-MCI criteria may be too broad, as substantial differences in frequencies of PD-MCI were observed with the application of differing criteria. Authors propose that a 1.5SD cut-off score below premorbid intellect may provide greater utility in characterizing PD-MCI than a 1.5SD cut-off below normative data, which has been widely applied in previous studies examining the MDS PD-MCI criteria.
01 January 2015
Vitamin D from different sources is inversely associated with Parkinson disease
Study data confirm the association between vitamin D deficiency and PD, and for the first time demonstrate an inverse association of 25(OH)D2 with PD. Given that 25(OH)D2 concentration is independent of sunlight exposure, this new finding suggests that the inverse association between vitamin D levels and PD is not simply attributable to lack of sunlight exposure in PD patients with impaired mobility. The current study, however, cannot exclude the possibility that gastrointestinal dysfunction, a non-motor PD
27 December 2014
Norepinephrine Deficiency in Parkinson's Disease: The Case for Noradrenergic Enhancement
In addition to reducing the consequences of deficient noradrenergic signaling, enhancement strate gies have the potential for augmenting the effects of dopaminergic therapies in PD. Furthermore, early recognition of the various clinical manifestations associated with NE deficiency, which may precede development of motor symptoms, could provide a window of opportunity for neuroprotective interventions.
15 December 2014
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