The brain-derived neurotrophic factor (BDNF) is a potent inhibitor of apoptosis-mediated cell death and neurotoxin-induced degeneration of dopaminergic neurons. There is a growing body of evidence implicating BDNF in the pathogenesis of Parkinson's disease (PD), suggesting it may eventually be used in the development of neuroprotective therapies for PD. The serum BDNF of 47 PD patients and of 23 control subjects was assessed, and serum BNDF levels were significantly decreased in PD patients when compared with controls (p = 0.046). Interestingly enough, BDNF correlated positively with a longer time span of the disease, as well as with the severity of the PD symptoms and with more advanced stages of the disease. Additionally, higher BDNF levels also correlated with poor balance as assessed by the Berg Balance Scale, more time spent at the Timed Up & Go Test, reduced speed of gait and shorter distance walked during the Six-Minute Walk Test. Our results corroborate the literature regarding the involvement of BDNF in PD. We hypothesize that lower BDNF levels in early stages of the disease may be associated with pathogenic mechanisms of PD. The increase of BDNF levels with the progression of the disease may be a compensatory mechanism in more advanced stages of PD.

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Leprosy, whose etiologic agent is Mycobacterium leprae, is an illness of ample clinical and immunopathological spectrum. Although chemokines seem to be involved in the immunopathogenesis of leprosis, few studies have been carried out to unveil the potential of chemokines as biological markers of the disease. The purpose of this study was to investigate the value of measuring CCL2, CCL3, CCL11 and CCL24 in plasma of patients with leprosy (LE) at different stages of multi-drug therapy (MDT). Chemokines were measured by ELISA in plasma of 30 non-infected individuals (NI) and 33 LE patients before and at different stages of treatment. The plasma concentration of CCL11 (p<0.01) and CCL24 (p<0.05) was increased in LE patients before treatment when compared to NI individuals. The plasma concentration of CCL24 decreased after MDT (p<0.05). No differences were observed in the concentration of CCL2 and CCL3 in plasma of NI and LE individuals. The elevated levels of CCL11 and CCL24 in plasma of patients with LE suggest that these chemokines may play a role in disease pathogenesis. Moreover, the decrease of CCL24 after treatment suggests that this chemokine might be useful as a biomarker of response to MDT in patients with leprosy.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in the survival of neurons and growth and differentiation of dendrites and axons. The purpose of the present study was to evaluate plasma levels of BDNF of leprosy patients at different stages of multidrug therapy (MDT) in comparison with non-infected individuals. Plasma levels of BDNF were measured by ELISA in 30 healthy controls and 37 leprosy patients at diagnosis, during and after MDT. Plasma levels of BDNF tended to be higher in control subjects in comparison with leprosy patients, but this difference does not reach statistical significance. Interestingly, BDNF levels changed following MDT, achieving statistical difference only at the 2 nd dose of MDT. These results indicate that BDNF may not be a surrogate marker of leprosy infection and/or related neuropathy. Further research is needed to investigate the meaning of BDNF level changes following leprosy treatment. Key words: leprosy, BDNF, peripheral neuropathy, biomarker, follow-up.Estudo do perfil da neurotrofina BDNF em casos novos de hanseníase antes, durante e após poliquimioterapia RESUMO O fator neurotrófico derivado do cérebro (BDNF) é uma neurotrofina envolvida na sobrevivência neuronal e no crescimento e diferenciação dos dendritos e axônios. O objetivo do presente estudo foi avaliar os níveis plasmáticos do BDNF de pacientes com hanseníase em diferentes fases da poliquimioterapia (PQT), em comparação com indivíduos não-infectados. Os níveis plasmáticos do BDNF foram mensurados pelo teste ELISA em 30 controles sadios e 37 pacientes com hanseníase no momento do diagnóstico, durante e após PQT. Os níveis plasmáticos do BDNF mostraram-se maiores nos indivíduos controles em comparação com os pacientes com hanseníase, mas não houve diferença estatisticamente significante. Curiosamente, os níveis de BDNF modificaram-se com o tratamento, mostrando diferença estatística apenas na segunda dose de PQT. Esses resultados indicam que o BDNF pode não ser um marcador de infecção na hanseníase e/ ou neuropatias relacionadas. Novas pesquisas são necessárias para investigar o significado das alterações nos níveis de BDNF ao longo do tratamento da hanseníase. Palavras-chave: hanseníase, BDNF, neuropatia periférica, biomarcador, seguimento.