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This is interesting in light of recent findings suggesting a genetic link between gba mutations and PD, and the role of several gene products associated with familial PD in mitophagy.
However, direct stimulation of primary motor cortex (M1) has recently been shown to be effective in reducing symptoms in PD, suggesting a role for cortex in patterning pathological rhythms.
A critical question concerning the molecular pathogenesis of PD is what role SNCA plays in sporadic PD.
Symptoms such as bradykinesia and hypokinesia seen in PD suggest a role in the selection of movement amplitude and speed based on energy requirements [56].
Based on biochemical findings in affected brain regions of PD patients a role of mitochondrial dysfunction and oxidative damage has been hypothesized in both ageing and neurodegeneration [42].
Previous studies of some members of this family found that they interact with PD and a role in the cell-to-cell and systemic transmission of redox signals have been suggested [59], [60].
In conclusion, DJ-1 and HSP70 might be therapeutic targets in PD for their role in counteracting oxidative stress and their involvement in α-syn solubility-related cell function.
Despite the potential importance of zinc in the pathogenesis of PD, its aetiological role remains largely unknown.
Dissimilar toxicities in that the toxicities of MS, IR, PD and the role of the aging process predate the development of overt T2DM.
In the current study, we further examined action-selection in PD, and the role of dopaminergic therapy and disease severity in behaviour.
47, 48 Hypertension was associated with reduced risk of PD, but the role of selective mortality in these individuals has not been studied.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com