Over the last twenty years, the Groebke-Blackburn-Bienaymé (GBB) reaction has been emerged as a powerful tool to access different nitrogen-based heterocycles as privileged scaffolds in medicinal chemistry. This multicomponent reaction is usually catalyzed by ordinary Brønsted or Lewis acid catalysts. Herein, we present a comparative study on the catalytic efficiencies of different rare earth triflates in GBB reactions under microwave heating, involving 2-aminopyridine or 2-aminothiazole, as aminoazole component, and different aldehydes and aliphatic isocyanides. The use of gadolinium(III) triflate as cheaper alternative catalyst for the most commonly used scandium(III) triflate was acknowledged for the first time, and a library of twenty three imidazo[1,2-a]pyridines and imidazo[2,1-b]thiazoles could be obtained in good to excellent yields.

Introdução A patogênese da doença de Parkinson (DP) envolve fatores ambientais e suscetibilidade genética, destacando-se a mutação de alfa-sinucleína (SNCA.)Objetivos Analisar a variante genética SNCA-A53T em pacientes com DP familiar (DPF) e DP esporádica (DPE).Método Foram estudados 294 indivíduos, independente de sexo, com etnia miscigenada, sendo 154 com DP e 140 sem a doença (grupo controle). A genotipagem deSNCA-A53T foi realizada por PCR/RFLP. Nível de significância para p < 0,05.Resultados Entre os pacientes, 37(24%) tinham DPF e 117 (75,9%) DPE. A ausência da mutação SNCA-A53T em todos os indivíduos.Conclusão DPE é destacada entre os pacientes, no entanto a mutaçãoSNCA-A53T ausente em todos os indivíduos, não diferenciando os grupo controle e pacientes, o que deve ser confirmado em população brasileira, considerando uma ampla casuística, além da ancestralidade.

Introduction The pathogenesis of Parkinson’s disease (PD) involves both genetic susceptibility and environmental factors, with focus on the mutation in thealpha-synucleingene (SNCA).Objective To analyse the polymorphism SNCA-A53T in patients with familial PD (FPD) and sporadic PD (SPD).Method A total of 294 individuals were studied, regardless of sex and with mixed ethnicity. The study group with 154 patients with PD, and the control group included 140 individuals without PD. The genotyping ofSNCA-A53T was performed by PCR/RFLP. Significance level was p < 0.05.Results Among all patients, 37 (24%) had FPD and 117 (75.9%) had SPD. The absence ofSNCA-A53T mutation was observed in all individuals.Conclusion SPD is notably observed in patients. However, the SNCA-A53T mutation was absent in all individuals, which does not differ controls from patients. This fact should be confirmed in a Brazilian study case with a more numerous and older population.

ObjetivoAnalisar a frequência do polimorfismo GSTP1-Alw26I, assim como estimar sua associação com substâncias tóxicas na doença de Parkinson (DP).MétodosA casuística avaliada foi composta por um grupo de estudo, com 154 pacientes, subdivididos em DP familial e esporádica, e outro com 158 idosos sem a doença (grupo controle). O polimorfismo GSTP1-Alw26I foi analisado por reação em cadeia da polimerase/polimorfismo de comprimento do fragmento de restrição (PCR/RFLP).ResultadosOs pacientes foram significativamente mais expostos a pesticidas, comparados com o grupo controle (p=0,0004), e o genótipo heterozigoto associado a exposição a pesticidas também prevaleceu nos pacientes (p=0,0001). O genótipo homozigoto selvagem apresentou relação com tabagismo (p=0,043) e etilismo (p=0,033) em pacientes com DP familial. Desse modo, a exposição a pesticidas está associada à DP, cujo efeito pode ser potencializado quando combinado ao genótipo heterozigoto de GSTP1-Alw26I. Estudos genético-ambientais envolvendo tabagismo, etilismo, GSTP1 e DP devem ser realizados em casuísticas numerosas, confirmando essa associação.

ObjectiveThis study aimed to analyze the frequency of GSTP1-Alw26I polymorphism and to estimate its association with toxic substances in Parkinson's disease (PD).MethodsA study group with 154 patients - subdivided into familial and sporadic PD groups - and 158 elderly individuals without the disease (control group) were evaluated. GSTP1-Alw26I polymorphism was analyzed by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP).ResultsPatients were significantly more exposed to pesticides compared with the control group (p=0.0004), and the heterozygote genotype associated to exposure to pesticides also prevailed in patients (p=0.0001). Wild homozygote genotype was related to tobacco use (p=0.043) and alcoholism (p=0.033) in familial PD patients.ConclusionExposure to pesticides is associated to PD, whose effect can be enhanced when combined with the heterozygote genotype of GSTP1-Alw26I. Also, large genetic and environmental studies considering tobacco use, alcoholism, GSTP1 and PD are necessary to confirm our findings.