Effects of Toxoplasma gondii on Levels of Interleukin-5 in Parkinson's Patients.

Parkinson's disease (PD) is a psychiatric neurological infection of the focal sensory system and is accepted as a multifactorial disease. Chronic Toxoplasmosis is sometimes associated with the proliferation of bradyzoites in the nervous system. The measurement of interleukin-5 (IL-5) as an inflammatory mediator in patients with PD and Toxoplasmosis infection may be helpful in determining the correlation between these diseases. In the present study, 80 examples were collected, including 35 patients diagnosed with idiopathic PD and 45 samples from healthy people from Najaf, Babylon, and Baghdad provinces, Iraq. After measuring the immunoglobulin G (IgG) antibody of Toxoplasma gondii, the level of IL-5 was evaluated in different groups. Serological examination showed that the IgG antibody of Toxoplasmosis increased (P<0.05) in people with PD (65.71%). Serum levels of IL-5 significantly decreased in people with PD. It is noteworthy that comparing serum levels of IL-5 between two groups of people with and without chronic Toxoplasmosis revealed that there was a significant decrease (P<0.05) in a concentration of serum IL-5 in individuals with chronic Toxoplasmosis. The current study confirmed the conceivable association between T. gondii and PD, and further research is recommended to explain the association between PD and Toxoplasmosis.

The Cataleptic, Asymmetric, Analgesic, and Brain Biochemical Effects of Parkinson's Disease Can Be Affected by Toxoplasma gondii Infection.

PURPOSE: Parkinson's disease (PD) is a neurodegenerative disorder with progressive motor defects. Therefore, the aim of the present investigation was to examine whether catalepsy, asymmetry, and nociceptive behaviors; the Nissl-body and neuron distribution; brain-derived neurotrophic factor (BDNF); malondialdehyde (MDA); total antioxidant capacity (TAC) levels; and the percentage of dopamine depletion of striatal neurons in the rat model of Parkinson's disease (PD) can be affected by Toxoplasma gondii (TG) infection. METHODS: Fifty rats were divided into five groups: control (intact rats), sham (rats which received an intrastriatal injection of artificial cerebrospinal fluid (ACSF)), PD control (induction of PD without TG infection), TG control (rats infected by TG without PD induction), and PD infected (third week after PD induction, infection by TG was done). PD was induced by the unilateral intrastriatal microinjection of 6-hydroxydopamine (6-OHDA) and ELISA quantified dopamine, BDNF, MDA, and TAC in the striatum tissue. Cataleptic, asymmetrical, nociceptive, and histological alterations were determined by bar test, elevated body swing test, formalin test, and Nissl-body and neuron counting in the striatal neurons. RESULTS: The results demonstrated that PD could significantly increase the number of biased swings, descent latency time, and nociceptive behavior and decrease the distribution of Nissl-stained neurons compared to the control and sham groups. TG infection significantly improved biased swing, descent latency time, nociceptive behavior, and the Nissl-body distribution in striatal neurons in comparison to the PD control group. The striatal level of BDNF in the PD-infected and TG control groups significantly increased relative to the PD control group. The striatal MDA was significantly higher in the PD control than other groups, while striatal TAC was significantly lower in the PD control than other groups. CONCLUSIONS: The current study indicates that TG infection could improve the cataleptic, asymmetric, nociceptive and behaviors; the level of striatal dopamine release; BDNF levels; TAC; and MDA in PD rats.

Cognitive Training and Noninvasive Brain Stimulation for Cognition in Parkinson's Disease: A Meta-analysis.

BACKGROUND: Many people with Parkinson's disease (PD) experience cognitive decline. It is not known whether cognitive training or noninvasive brain stimulation are effective at alleviating cognitive deficits in PD. OBJECTIVE: To examine cognitive training and non-invasive brain stimulation interventions for cognition in PD. METHODS: An extensive search was conducted of published and unpublished studies in online databases. Studies were selected if they were controlled trials examining standard (not individualized) or tailored (individualized) cognitive training, repetitive transcranial magnetic stimulation (rTMS), or transcranial direct current stimulation (tDCS) in PD, with outcomes measured by standardized neuropsychological tests. RESULTS: Fourteen controlled trials met inclusion criteria. For executive function, the pooled effect size (Hedges' g) for cognitive training (standard and tailored combined) was small ( g = 0.42) but statistically significant (95% CI 0.15-0.68). The pooled effect for standard cognitive training (alone) was medium ( g = 0.51) and significant (95% CI 0.16-0.85). For attention/working memory, small pooled effect sizes were found when combining standard and tailored cognitive training ( g = 0.23; 95% CI 0.02-0.44) and for standard cognitive training alone ( g = 0.29; 95% CI 0.04-0.53), both significant. For memory, small but significant pooled effect sizes were also found when combining standard and tailored cognitive training and for standard cognitive training alone. CONCLUSIONS: The results suggest that standard and tailored cognitive training may improve executive function, attention/working memory, and memory in PD. Future studies must adopt randomized controlled trial designs to explore the therapeutic potential of these interventions.

Toxocara seroprevalence in patients with idiopathic Parkinson's disease: chance association or coincidence?

Most cases of idiopathic Parkinson disease (IPD) are believed to be due to a combination of genetic and environmental factors. The purpose of this study is to investigate the relationship between toxocariasis and Parkinson disease (PD). Patients were selected from people who were admitted to the Movement Disorders Branch, Neurology Department of Elazig University Faculty of Medicine Elazig, Turkey. We studied specific IgG antibodies against Toxocara canis (T. canis) in 50 patients with idiopathic Parkinson and 50 healthy volunteers. We investigated the clinical history of three patients infected with T. canis. We also studied specific IgG antibodies against Toxoplasma gondii in these groups. Antibodies anti-Toxocara canis were found in 3 idiopathic PD (6%) (P = 0.121) and antibody titer was not found in control. A patient had history of the presence of dog in current dog ownership. We did not detect any statistically significant association between T. canis and IPD. But, we believe that further comprehensive studies are required for understanding whether there is a causal relation between toxocariasis and PD. We didn't find possible association between Toxoplasma gondii and IPD (P = 0.617).

The probable relation between Toxoplasma gondii and Parkinson's disease.

Parkinson's disease (PD), a chronic progressive neurodegenerative disorder, has a mainly unknown multifactorial etiology. Neuroinflammatory mechanisms might contribute to the cascade of events leading to neuronal degeneration. Toxoplasmosis can be associated with various neuropsychiatric disorders. The most commonly affected central nervous system (CNS) region in toxoplasmosis is the cerebral hemisphere, followed by the basal ganglia, cerebellum and brain stem. Therefore, in this study, we aimed to investigate the possible association between Toxoplasma infection and PD by evaluating the serum anti-Toxoplasma gondii IgG antibodies. There were no difference between the socioeconomic status of the patients and control subjects and magnetic resonance images of the patients were normal. Serum anti-T. gondii IgG levels were measured using ELISA. There was no statistically significant differences among the patients and control subjects with respect to age (66.01+/-12.14 years, 62.42+/-5.93 years, p=0.089; respectively) and gender. The sero-positivity rate for anti-T. gondii IgG antibodies in PD patients and control groups were 42.3 and 22.5%, respectively, and they were statistically significant (p=0.006). These results suggest that Toxoplasma infection may be involved in the pathogenetic mechanisms of PD. If confirmed, this hypothesis would represent a valuable advancement in care of patients with Parkinson's disease.

Efficacy of rivastigmine for cognitive symptoms in Parkinson disease with dementia.

BACKGROUND: Impairment of multiple neurotransmitter networks, including acetylcholine, may contribute to the cognitive impairment in patients with Parkinson disease with dementia (PDD). Therefore, cholinesterase inhibitors might improve cognitive function in PDD. On the other hand, enhancing cholinergic function could plausibly worsen features of parkinsonism. OBJECTIVE: To determine if oral cholinesterase inhibitors improve measures of cognitive outcome and are tolerated by people with PDD. METHODS: We addressed the question through the development of a critically appraised topic. Participants included consultant and resident neurologists, clinical epidemiologists, a medical librarian, and behavioral neurology and movement disorder specialists. Participants began with a structured clinical question, devised search strategies, compiled the best evidence, performed a critical appraisal, summarized the evidence, provided commentary, and declared bottom-line conclusions. RESULTS: A randomized controlled trial (n = 541) showed that, compared with placebo, rivastigmine (mean, 8.6 mg/d) significantly improved scores on 2 coprimary cognitive outcome scales in PDD, including the Alzheimer disease Cooperative Study-Clinician's Global Impression of Change. When dichotomized to evaluate clinically significant benefit (moderate or marked improvement), this outcome was not significant (risk difference = 5.3%; 95% confidence interval (CI) = -1.6 to 12.1). The number needed to treat (NNT) to avoid clinically significant worsening of cognition was 10 (95% CI = 6-28). The NNT for the combined outcome of either achieving clinically significant benefit or avoiding significant worsening was 7. The numbers needed to harm for cholinergic side effects were 9 (95% CI = 5-24) for parkinsonian symptoms and 11 (95% CI = 6-32) for rivastigmine discontinuation due to any side effect. CONCLUSION: Rivastigmine therapy for PDD is associated with significant tradeoffs in efficacy and adverse effects. Carefully monitored trials of rivastigmine may provide meaningful benefits for a minority of PDD patients.

Ipsilateral sequential arm movements after unilateral subthalamic deep-brain stimulation in patients with Parkinson's disease.

Unilateral STN-DBS significantly improves the performance of contralateral sequential arm movements. Whether unilateral STN-DBS also improves ipsilateral sequential movement is unclear. In this study in unmedicated parkinsonian patients, we tested the effect of unilateral STN-DBS on the performance of ipsilateral sequential movements and compared it with the performance of contralateral sequential movements. Three-dimensional movements were recorded with the ELITE system and three kinematic variables were considered: total movement time (TMT), total inter-onset latency (IOL), and spatial accuracy. Unilateral STN-DBS significantly decreased TMT in the contralateral arm and only tended to do so also in the ipsilateral arm, whereas it significantly decreased IOL and worsened spatial accuracy only on the contralateral side. Before unilateral STN-DBS a positive correlation was present between the clinical impairment and the TMTs in the contralateral and ipsilateral sides. After unilateral STN-DBS the UPDRS scores improved in the contralateral and to a lesser extent also in the ipsilateral side. Correlation analysis between clinical and kinematic data showed no differences between the contralateral and ipsilateral sides. Our kinematic findings show that after STN-DBS parkinsonian patients' performance of a sequential motor task improves significantly on the contralateral but only tended to do so on the ipsilateral side. Ipsilateral changes can be explained by the observation that the output structures of the basal ganglia send large ipsilateral and less dense contralateral projections to the thalamus.

Parkinsonism in a patient with AIDS and cerebral opportunistic granulomatous lesions.

The localization of opportunistic infections in the basal ganglia in patients with acquired immunodeficiency syndrome (AIDS) can cause movement disorders, such as choreoathetosis, dystonia, hemiballism and, more rarely, parkinsonism. We describe the case of an AIDS patient who developed cerebral opportunistic granulomatous lesions and, subsequently, a parkinsonian akinetic-rigid syndrome. In agreement with cases reported in the literature, the parkinsonian syndrome developed only when the lesions bilaterally involved basal ganglia. The critical localization of the opportunistic lesions in the direct and indirect strio-pallidal pathways possibly associated with the HIV-related neurotoxicity might have contributed to determine this clinical picture.

The experience of living with Parkinson's disease.

This phenomenological study examined the experience of living with Parkinson's disease. Data were collected from six individuals during open-ended interviews conducted in subjects' homes. Interviews were tape recorded, transcribed verbatim and then subjected to content analysis. Four themes emerged from data analysis. The experience of living with Parkinson's disease involved impact of the disease, dealing with the disease, maintaining independence and normality, and effort. Impact of the disease involved personal losses of mobility and social activity. The perceived loss of independence and normality resulted in a changed self-concept. Dealing with the disease involved specific strategies and resources such as health and social support. The goal which kept subjects going was to maintain independence and normality. The overriding theme was effort; effort was involved in every aspect of life with Parkinson's disease. Implications for nursing practice and research are discussed.