Agricultural work and reduced circulating uric acid are both associated with initial hospital admission for Parkinson’s disease

AbstractMonoamine oxidase type B inhibitors act in Parkinson’s disease (PD) via potentiation of dopamine, but may also have neuroprotective effects by reducing oxidative damage. Oxidative damage is also a feature of environmental toxins, including pesticides, that are an established risk factor for PD. Another risk factor is low circulating uric acid (UA), which may relate to UA being the major endogenous antioxidant in the human body. We have undertaken a study of 192 initial admissions for PD in a general hospital neurology department in a partly rural region of Southern China to determine if there is an increased rate of PD in agricultural workers who have a high risk of exposure to pesticides, and how it may relate to deficits in UA. We found a disproportionately high number of agricultural workers admitted with PD (66.7% vs. 54.3% of all neurology admissions) and that PD subjects have a substantial reduction in UA. This is further reduced in agricultural workers and thus may contribute to the increased vulnerability of this group to PD.

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Confirmation of LRRK2 S1647T variant as a risk factor for Parkinson’s disease in Southern China

European Journal of Neurology ◽

10.1111/j.1468-1331.2010.03164.x ◽

2011 ◽

Vol 18 (3) ◽

pp. 538-540 ◽

Cited By ~ 10

Author(s):

Y. Zheng ◽

Y. Liu ◽

Q. Wu ◽

H. Hong ◽

H. Zhou ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Risk Factor ◽

Southern China

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Neuroprotective Effects of Pomegranate Juice against Parkinson’s Disease and Presence of Ellagitannins-Derived Metabolite—Urolithin A—In the Brain

International Journal of Molecular Sciences ◽

10.3390/ijms21010202 ◽

2019 ◽

Vol 21 (1) ◽

pp. 202 ◽

Cited By ~ 17

Author(s):

Małgorzata Kujawska ◽

Michael Jourdes ◽

Monika Kurpik ◽

Michał Szulc ◽

Hanna Szaefer ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Oxidative Damage ◽

Control Level ◽

Experimental Studies ◽

Pomegranate Juice ◽

Neuroprotective Effects ◽

Urolithin A ◽

Wide Range ◽

The Brain

Pomegranate juice is a rich source of ellagitannins (ETs) believed to contribute to a wide range of pomegranate’s health benefits. While a lot of experimental studies have been devoted to Alzheimer disease and hypoxic-ischemic brain injury, our knowledge of pomegranate’s effects against Parkinson’s disease (PD) is very limited. It is suggested that its neuroprotective effects are mediated by ETs-derived metabolites—urolithins. In this study, we examined the capability of pomegranate juice for protection against PD in a rat model of parkinsonism induced by rotenone. To evaluate its efficiency, assessment of postural instability, visualization of neurodegeneration, determination of oxidative damage to lipids and α-synuclein level, as well as markers of antioxidant defense status, inflammation, and apoptosis, were performed in the midbrain. We also check the presence of plausible active pomegranate ETs-derived metabolite, urolithin A, in the plasma and brain. Our results indicated that pomegranate juice treatment provided neuroprotection as evidenced by the postural stability improvement, enhancement of neuronal survival, its protection against oxidative damage and α-synuclein aggregation, the increase in mitochondrial aldehyde dehydrogenase activity, and maintenance of antiapoptotic Bcl-xL protein at the control level. In addition, we have provided evidence for the distribution of urolithin A to the brain.

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Oxidative damage in Parkinson's disease

PsycEXTRA Dataset ◽

10.1037/e429352005-001 ◽

2003 ◽

Author(s):

M. Flint Beal ◽

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Oxidative Damage

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Nanoemulsion Improves the Neuroprotective Effects of Curcumin in an Experimental Model of Parkinson’s Disease

Neurotoxicity Research ◽

10.1007/s12640-021-00362-w ◽

2021 ◽

Author(s):

Osmar Vieira Ramires Júnior ◽

Barbara da Silva Alves ◽

Paula Alice Bezerra Barros ◽

Jamile Lima Rodrigues ◽

Shana Pires Ferreira ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Experimental Model ◽

Neuroprotective Effects

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Effectiveness and mechanisms of adipose-derived stem cell therapy in animal models of Parkinson’s disease: a systematic review and meta-analysis

Translational Neurodegeneration ◽

10.1186/s40035-021-00238-1 ◽

2021 ◽

Vol 10 (1) ◽

Author(s):

Keya Li ◽

Xinyue Li ◽

Guiying Shi ◽

Xuepei Lei ◽

Yiying Huang ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Animal Models ◽

Therapeutic Option ◽

Meta Analysis ◽

Future Application ◽

Neuroprotective Effects ◽

Standard Mean Difference ◽

Study Characteristics

AbstractAnimal models provide an opportunity to assess the optimal treatment way and the underlying mechanisms of direct clinical application of adipose-derived stem cells (ADSCs). Previous studies have evaluated the effects of primitive and induced ADSCs in animal models of Parkinson’s disease (PD). Here, eight databases were systematically searched for studies on the effects and in vivo changes caused by ADSC intervention. Quality assessment was conducted using a 10-item risk of bias tool. For the subsequent meta-analysis, study characteristics were extracted and effect sizes were computed. Ten out of 2324 published articles (n = 169 animals) were selected for further meta-analysis. After ADSC therapy, the rotation behavior (10 experiments, n = 156 animals) and rotarod performance (3 experiments, n = 54 animals) were improved (P < 0.000 01 and P = 0.000 3, respectively). The rotation behavior test reflected functional recovery, which may be due to the neurogenesis from neuronally differentiated ADSCs, resulting in a higher pooled effect size of standard mean difference (SMD) (− 2.59; 95% CI, − 3.57 to − 1.61) when compared to that of primitive cells (− 2.18; 95% CI, − 3.29 to − 1.07). Stratified analyses by different time intervals indicated that ADSC intervention exhibited a long-term effect. Following the transplantation of ADSCs, tyrosine hydroxylase-positive neurons recovered in the lesion area with pooled SMD of 13.36 [6.85, 19.86]. Transplantation of ADSCs is a therapeutic option that shows long-lasting effects in animal models of PD. The potential mechanisms of ADSCs involve neurogenesis and neuroprotective effects. The standardized induction of neural form of transplanted ADSCs can lead to a future application in clinical practice.

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Neuroprotective Effects of a GLP-2 Analogue in the MPTP Parkinson’s Disease Mouse Model

Journal of Parkinson s Disease ◽

10.3233/jpd-202318 ◽

2021 ◽

pp. 1-15

Author(s):

Zijuan Zhang ◽

Li Hao ◽

Ming Shi ◽

Ziyang Yu ◽

Simai Shao ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Substantia Nigra ◽

Mouse Model ◽

Neurodegenerative Disorder ◽

Enzyme Linked Immunosorbent Assay ◽

Protective Effects ◽

Neuroprotective Effects ◽

Expression Levels ◽

Dual Agonist

Background: Glucagon-like peptide 2 (GLP-2) is a peptide hormone derived from the proglucagon gene expressed in the intestines, pancreas and brain. Some previous studies showed that GLP-2 improved aging and Alzheimer’s disease related memory impairments. Parkinson’s disease (PD) is a progressive neurodegenerative disorder, and to date, there is no particular medicine reversed PD symptoms effectively. Objective: The aim of this study was to evaluate neuroprotective effects of a GLP-2 analogue in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) PD mouse model. Methods: In the present study, the protease resistant Gly(2)-GLP-2 (50 nmol/kg ip.) analogue has been tested for 14 days by behavioral assessment, transmission electron microscope, immunofluorescence histochemistry, enzyme-linked immunosorbent assay and western blot in an acute PD mouse model induced by MPTP. For comparison, the incretin receptor dual agonist DA5-CH was tested in a separate group. Results: The GLP-2 analogue treatment improved the locomotor and exploratory activity of mice, and improved bradykinesia and movement imbalance of mice. Gly(2)-GLP-2 treatment also protected dopaminergic neurons and restored tyrosine hydroxylase expression levels in the substantia nigra. Gly(2)-GLP-2 furthermore reduced the inflammation response as seen in lower microglia activation, and decreased NLRP3 and interleukin-1β pro-inflammatory cytokine expression levels. In addition, the GLP-2 analogue improved MPTP-induced mitochondrial dysfunction in the substantia nigra. The protective effects were comparable to those of the dual agonist DA5-CH. Conclusion: The present results demonstrate that Gly(2)-GLP-2 can attenuate NLRP3 inflammasome-mediated inflammation and mitochondrial damage in the substantia nigra induced by MPTP, and Gly(2)-GLP-2 shows neuroprotective effects in this PD animal model.

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