ABSTRACT
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.
Subject(s)
Behavior, Animal/physiology , Parkinson Disease , Toxoplasmosis , Animals , Brain Chemistry , Catalepsy/physiopathology , Corpus Striatum/cytology , Corpus Striatum/metabolism , Corpus Striatum/parasitology , Corpus Striatum/pathology , Disease Models, Animal , Dopamine/metabolism , Male , Neurons/cytology , Nociception/physiology , Parkinson Disease/metabolism , Parkinson Disease/parasitology , Parkinson Disease/physiopathology , Rats , Rats, Sprague-Dawley , Toxoplasmosis/metabolism , Toxoplasmosis/physiopathologyABSTRACT
Histopathology and quantitative PCR (qPCR) were used to determine the tissue distribution of Neospora caninum in calves at 80 days postinfection. Our findings revealed that the most appropriate brain areas for researching N. caninum pathogenesis were the amygdala and hippocampus for qPCR and the corpus striatum and diencephalon for histopathology.
Subject(s)
Amygdala/parasitology , Coccidiosis/veterinary , Corpus Striatum/parasitology , Diencephalon/parasitology , Hippocampus/parasitology , Neospora , Animals , Antibodies, Protozoan/immunology , Cattle , Cattle Diseases/mortality , Cattle Diseases/parasitology , DNA, Protozoan/isolation & purification , Male , Neospora/genetics , Neospora/immunology , Neospora/pathogenicity , Tissue DistributionSubject(s)
AIDS-Related Opportunistic Infections/complications , Parkinson Disease, Secondary/etiology , Toxoplasmosis, Cerebral/complications , Corpus Striatum/parasitology , Corpus Striatum/pathology , Encephalitis/complications , Encephalitis/microbiology , Encephalitis/virology , Humans , Magnetic Resonance Imaging , Parkinson Disease, Postencephalitic/etiology , Parkinson Disease, Secondary/parasitology , Parkinson Disease, Secondary/pathology , Toxoplasmosis, Cerebral/pathologyABSTRACT
We studied a Japanese patient who developed parkinsonian symptoms over 3 months before the diagnosis of acquired immunodeficiency syndrome. Brain MRI showed multiple lesions with mass effect and ring enhancement in the basal ganglia and subcortical white matter suggesting Toxoplasma infection. Anti-Toxoplasma therapy and highly active antiretroviral therapy for 6 months allowed improvement of parkinsonism, brain MRI findings, and immune system.