2020
DOI: 10.1016/j.jep.2019.112213
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Ginseng protein protects against mitochondrial dysfunction and neurodegeneration by inducing mitochondrial unfolded protein response in Drosophila melanogaster PINK1 model of Parkinson's disease

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Cited by 54 publications
(33 citation statements)
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“…In the future, considering the specific properties of TCM compounds identified in this study, it would be interesting to investigate whether combination of TCM HEs increase protection in HD models. During the course of our study, Liu et al demonstrated that ginseng treatment delays the onset of a Parkinson-like phenotype in PINK1 depleted flies [49]. Together with our study, this suggests that TCM HEs may be useful on an extended panel of age-related neurodegenerative diseases and should motivate new studies on available Drosophila models before extension to mice models.…”
Section: Discussionsupporting
confidence: 79%
“…In the future, considering the specific properties of TCM compounds identified in this study, it would be interesting to investigate whether combination of TCM HEs increase protection in HD models. During the course of our study, Liu et al demonstrated that ginseng treatment delays the onset of a Parkinson-like phenotype in PINK1 depleted flies [49]. Together with our study, this suggests that TCM HEs may be useful on an extended panel of age-related neurodegenerative diseases and should motivate new studies on available Drosophila models before extension to mice models.…”
Section: Discussionsupporting
confidence: 79%
“…The modulation of the UPR by α-syn is not restricted to neurons since mutated α-syn was shown to activate the PERK axis in astrocytes [ 128 ]. Considering that astrocytes are involved in various brain functions and support neuronal activity, an activation of UPR by α-syn in these cells may lead to deleterious consequences.…”
Section: Implication Of the Er Upr In Pd Pathologymentioning
confidence: 99%
“…Oxidative Medicine and Cellular Longevity mitochondrial dysfunction (particularly oxidative stress) has been demonstrated to contribute to the pathogenesis of PD by multiple lines of evidence both in PD patients and related animal models [33][34][35] (Figure 1). MPTP, a synthetic opioid drug produced during the manufacture of 1-methyl-4-phenyl-4-propionoxypiperidine (MPPP), interferes with the components of the mitochondria electron transport chain (ETC) to be transformed into a toxic cation named 1-methyl-4-phenylpyridinium (MPP + ) via a monoamine oxidase B enzymatic action [36].…”
Section: Mitochondrial Dysfunctionmentioning
confidence: 99%