Parkinson's disease (PD) is characterized by progressive motor impairment attributed to progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta. In addition to an accumulation of iron, there is also an increased production of reactive oxygen/nitrogen species (ROS/RNS) and inflammatory markers. These observations suggest that iron dyshomeostasis may be playing a key role in neurodegeneration. However, the mechanisms underlying this metal-associated oxidative stress and neuronal damage have not been fully elucidated. To determine peripheral levels of iron, ferritin, and transferrin in PD patients and its possible relation with oxidative/nitrosative parameters, whilst attempting to identify a profile of peripheral biomarkers in this neurological condition. Forty PD patients and 46 controls were recruited to compare serum levels of iron, ferritin, transferrin, oxidative stress markers (superoxide dismutase (SOD), catalase (CAT), nitrosative stress marker (NOx), thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP) and vitamin C) as well as inflammatory markers (NTPDases, ecto-5’-nucleotidase, adenosine deaminase (ADA), ischemic-modified albumin (IMA) and myeloperoxidase). Iron levels were lower in PD patients, whereas there was no difference in ferritin and transferrin. Oxidative stress (TBARS and AOPP) and inflammatory markers (NTPDases, IMA, and myeloperoxidase) were significantly higher in PD, while antioxidants FRAP, vitamin C, and non-protein thiols were significantly lower in PD. The enzymes SOD, CAT, and ecto-5’-nucleotidase were not different among the groups, although NOx and ADA levels were significantly higher in the controls. Our data corroborate the idea that ROS/RNS production and neuroinflammation may dysregulate iron homeostasis and collaborate to reduce the periphery levels of this ion, contributing to alterations observed in the pathophysiology of PD.

The present results should be considered as positive preliminary evidence. Further studies are needed to determine the association between ADORA2A and dyskinesia. Original submitted 3 December 2014; Revision submitted 13 February 2015.

Background: Multiple studies have suggested that various pesticides are associated with a higher risk of developing Parkinson's disease (PD) and may influence the progression of the disease. However, the evidence regarding the impact of pesticide exposure on mortality among patients with PD is equivocal. This study examines whether pesticide exposure influences the risk of mortality among patients with PD in Southern Brazil. Methods: A total of 150 patients with idiopathic PD were enrolled from 2008 to 2013 and followed until 2019. In addition to undergoing a detailed neurologic evaluation, patients completed surveys regarding socioeconomic status and environmental exposures. Results: Twenty patients (13.3%) reported a history of occupational pesticide exposure with a median duration of exposure of 10 years (mean = 13.1, SD = 11.2). Patients with a history of occupational pesticide exposure had higher UPDRS-III scores, though there were no significant differences in regards to age, sex, disease duration, Charlson Comorbidity Index, and age at symptom onset. Patients with occupational pesticide exposure were more than twice as likely to die than their unexposed PD counterparts (HR = 2.32, 95% CI [1.15, 4.66], p = 0.018). Occupational pesticide exposure was also a significant predictor of death in a cox-proportional hazards model which included smoking and caffeine intake history (HR = 2.23, 95% CI [1.09, 4.59], p = 0.03)) and another which included several measures of socioeconomic status (HR = 3.91, 95% CI [1.32, 11.58], p = 0.01). Conclusion: In this prospective cohort study, we found an increased all-cause mortality risk in PD patients with occupational exposure to pesticides. More studies are needed to further analyze this topic with longer follow-up periods, more detailed exposure information, and more specific causes of mortality.

Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.

Stroke-like migraine attacks after radiation therapy (SMART) syndrome is a rare late complication of brain irradiation. Patients commonly present recurrent attacks of headaches, seizures, and paroxysmal focal neurological deficits including aphasia, negligence, or hemianopsia. We report a 41-year-old male patient admitted to our emergency room with a reduced level of consciousness and global aphasia. One month prior to admission, he started with frequent headache attacks of moderate intensity and paroxysmal behavioral alterations, advancing to confusion, gait instability, language impairment, and somnolence. He had a history of medulloblastoma treated with surgical resection followed by craniospinal irradiation 21 years before symptom onset. After excluding more frequent causes for the patient’s symptoms along with a suggestive image pattern, we started treatment for SMART syndrome with high-dose corticosteroid and calcium channel blocker verapamil. The patient gradually improved his level of consciousness and recovered from aphasia and gait instability without new seizures or neuropsychiatric symptoms. Follow-up brain magnetic resonance imaging showed resolution of the typical findings. This case displays a successful clinical evolution of a patient treated for SMART syndrome in which identification of previous radiation treatment, exclusion of other etiologies, and prompt treatment institution were key for effectively tackling this disease.

Background: Multiple studies have suggested that various pesticides are associated with a higher risk of developing Parkinson’s disease (PD) and may influence the progression of the disease. However, the evidence regarding the impact of pesticide exposure on mortality among patients with PD is equivocal. This study examines whether pesticide exposure influences the risk of mortality among patients with PD in Southern Brazil. Methods: A total of 150 patients with idiopathic PD were enrolled from 2008-2013 and followed until 2019. In addition to undergoing a detailed neurologic evaluation, patients completed surveys regarding socioeconomic status and environmental exposures. Results: Twenty patients (13.3%) reported a history of occupational pesticide exposure with a median duration of exposure of 10 years (mean = 13.1, SD = 11.2). Patients with a history of occupational pesticide exposure had higher UPDRS-III scores, though there were no significant differences in regards to age, sex, disease duration, Charlson Comorbidity Index, and age at symptom onset. Patients with occupational pesticide exposure were more than twice as likely to die than their unexposed PD counterparts (HR = 2.32, 95% CI [1.15, 4.66], p = 0.018). Occupational pesticide exposure was also a significant predictor of death in a cox-proportional hazards model which included smoking and caffeine intake history (HR = 2.29, 95% CI [1.13, 4.63], p = 0.02) and another which included several measures of socioeconomic status (HR = 3.92, 95% CI [1.41, 10.90], p = 0.009).Conclusion: In this prospective cohort study, we found an increased all-cause mortality risk in PD patients with occupational exposure to pesticides. More studies are needed to further analyze this topic with longer follow-up periods, more detailed exposure information, and more specific causes of mortality.

Introduction: Coffee has been inversely associated with Parkinson's disease (PD) in many studies, and caffeine is the leading candidate to mediate this effect. Mate (Ilex paraguariensis, IP), a caffeinated beverage rich in antioxidants consumed in South America, was also inversely associated with PD in one study from Argentina. Other varieties of IP infusion, such as chimarrão, were never studied in PD. Chimarrão is a common caffeinated beverage consumed in Brazil made with the leaves and stems of IP.Methods: A case–control study was conducted to evaluate the relationship between chimarrão ingestion and PD in southern Brazil. All subjects answered a questionnaire about the frequency of chimarrão and coffee intake. A multiple regression analysis adjusted for age and sex was performed to assess the association between PD and chimarrão consumption.Results: We included 200 PD patients and 200 healthy controls. High consumption of chimarrão was inversely associated with PD (OR = 0.44, 95% CI = 0.24–0.81, P = 0.008). High consumption of coffee was also inversely associated with PD, as expected. Chimarrão remained associated when adjusted for coffee consumption, smoking history, and age (OR 0.46, 95% CI = 0.25–0.86, P = 0.014). These two exposures showed an additive effect.Conclusion:Chimarrão consumption was inversely associated with PD, even after adjusting for coffee intake, suggesting a possible protective role. IP's effect can be mediated by caffeine and through its antioxidant components. Chimarrão has a lower concentration of caffeine compared with coffee and has numerous substances with antioxidative effects that may be important to PD protection. Further studies are needed to test this hypothesis.

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