Navegando por Palavras-chave "parkinsonism"
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- ItemSomente MetadadadosAvaliação do efeito neuroprotetor da cafeína em modelo experimental de doença de parkinson: um estudo comportamental, neuroquímico e imunohistoquímico(Universidade Federal de São Paulo (UNIFESP), 2013-12-20) Machado Filho, Joao Ananias [UNIFESP]; Cavalheiro, Esper Abrao Cavalheiro [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. The occurrence of clinical symptoms is related to the loss of approximately 80% of striatal dopamine and 50% of nigral neurons. Caffeine (CAF) is a methylxanthine with extensive use in medicines and products such as coffee, tea and chocolates, and being assigned neuroprotective activities. This study evaluated neuroprotective effects of caffeine in an animal model of PD induced by 6 - OHDA through behavioral studies, neurochemical and immunohistochemical studies. The animals, male Wistar rats (250-300g) were subjected to three protocols (P1, P2, P3) of striatal lesion by 6-OHDA, with concentration of 24μg/2μL in P1, and 12μg/2μL in P2 and P3. The preventive and curative treatment was done as follows in the these protocols: P1 - CAF treatment (10 and 20mg/kg) for two weeks after the injury (curative); P2 - CAF treatment (10 and 20mg/kg) for two weeks after the injury (curative); another group was treated with CAF (10 mg/kg) and L-Dopa (10mg/kg) after injury (curative); P3 - treated with CAF (5, 10 and 20mg/kg) for two weeks prior to the injury (prophylactic) and continued for two weeks after the injury (curative). The results demonstrate that the 6- OHDA caused an increase in the number of contralateral rotations induced by apomorphine and reduction of striatal dopamine levels with the degree of lesion probably directly related to the dose of 6-OHDA. These effects were reversed by the administration of CAF (10 and 20mg/kg) in P1 and P2, besides being observed increased neuronal viability and immunohystochemical changes that, together, denote neuroprotective activity of CAF in this model. Co-administration of levodopa (10 mg/kg) and CAF (10mg/kg) showed no effect on striatal dopamine concentrations beyond those already observed in the treatment with isolated CAF. CAF (20mg/kg) produced a significant increase in dopamine levels in sham animals and animals lesioned with 6-OHDA. Preventive treatment with caffeine (P3) showed similar results to curative treatment (P2) as observed in the neurochemical and behavioral assessments. Thus, it was demonstrated the neuroprotective effect of caffeine in this experimental study, presenting itself as a potential substance for the prevention and treatment of Parkinson's disease.
- ItemAcesso aberto (Open Access)C9orf72-related disorders: expanding the clinical and genetic spectrum of neurodegenerative diseases(Assoc Arquivos Neuro- Psiquiatria, 2015-03-01) Souza, Paulo Victor Sgobbi de [UNIFESP]; Pinto, Wladimir Bocca Vieira de Rezende [UNIFESP]; Oliveira, Acary Souza Bulle [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Neurodegenerative diseases represent a heterogeneous group of neurological conditions primarily involving dementia, motor neuron disease and movement disorders. They are mostly related to different pathophysiological processes, notably in family forms in which the clinical and genetic heterogeneity are lush. in the last decade, much knowledge has been acumulated about the genetics of neurodegenerative diseases, making it essential in cases of motor neuron disease and frontotemporal dementia the repeat expansions of C9orf72 gene. This review analyzes the main clinical, radiological and genetic aspects of the phenotypes related to the hexanucleotide repeat expansions (GGGGCC) of C9orf72 gene. Future studies will aim to further characterize the neuropsychological, imaging and pathological aspects of the extra-motor features of motor neuron disease, and will help to provide a new classification system that is both clinically and biologically relevant.
- ItemSomente MetadadadosChediak-Higashi syndrome with parkinsonism(Wiley-Blackwell, 2004-04-01) Silveira-Moriyama, L.; Moriyama, T. S.; Gabbi, TVB; Ranvaud, R.; Barbosa, E. R.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)Chediak-Higashi syndrome (CHS), typically presents with partial albinism and severe hematological abnormalities. About 10% of the patients have a mild adult form associated with various neurological manifestations. We describe the case of a 24-year-old woman with parkinsonism that responded well to antiparkinsonian drugs. (C) 2004 Movement Disorder Society.
- ItemAcesso aberto (Open Access)Depression increases in patients with Parkinson?s disease according to the increasing severity of the cognitive impairment(Academia Brasileira de Neurologia - ABNEURO, 2014-06-01) Chagas, Marcos Hortes N.; Moriyama, Tais Silveira [UNIFESP]; Felício, André Carvalho [UNIFESP]; Sosa, Ana Luisa; Bressan, Rodrigo Affonseca [UNIFESP]; Ferri, Cleusa Pinheiro [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Hospital Israelita Albert Einstein Instituto Israelita de Ensino e Pesquisa; National Institute of Neurology and Neurosurgery of MéxicoObjective : To test the hypothesis that severity of cognitive impairment modifies the association between depression and Parkinson’s disease (PD). Method : One-phase population-based door-to-door surveys. This is a secondary analysis of 1,451 people aged 65 years and older with cognitive impairment living in defined catchment areas. Depression was estimated according to ICD-10, self-reported PD, disability according to WHODAS-II and cognitive status according to the CSI-D. Results : The mean age of the sample was 79.3 years old and most (69%) were women. Of the total sample, 16.1% had depression and it was significantly higher among participants with PD. There was an increase on the ORs of the association between depression and PD with decreased scores in the cognitive test (Adjusted OR from 0.98 to 8.04). Conclusion : The association between depression and PD increases with the severity of the cognitive impairment.
- ItemSomente MetadadadosOlfactory Heterogeneity in LRRK2 Related Parkinsonism(Wiley-Blackwell, 2010-12-15) Silveira-Moriyama, Laura; Munhoz, Renato Pupi; Carvalho, Margarete de J.; Raskin, Salmo; Rogaeva, Ekaterina; Aguiar, Patricia de C.; Bressan, Rodrigo A. [UNIFESP]; Felicio, Andre C. [UNIFESP]; Barsottini, Orlando G. P. [UNIFESP]; Andrade, Luiz Augusto Franco de [UNIFESP]; Chien, Hsin F.; Bonifati, Vincenzo; Barbosa, Egberto R.; Teive, Helio A.; Lees, Andrew J.; UCL; Univ Fed Parana; Universidade de São Paulo (USP); Univ Toronto; Hosp Israelita Albert Einstein; Universidade Federal de São Paulo (UNIFESP); Erasmus MCLRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy-body pathology at post-mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS-16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. the mean SS-16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for beta = -4.7 to -1.7) and lower than in controls (p = 0.007, 95% CI for beta = +0.6 to +3.6). in the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. (C) 2010 Movement Disorder Society