RESUMO
INTRODUCTION: Huntington's Disease (HD) is a genetic neurodegenerative disease for which there is currently no disease-modifying treatment. One of several underlying mechanisms proposed to be involved in HD pathogenesis is inflammation; there is now accumulating evidence that the immune system may play an integral role in disease pathology and progression. As such, modulation of the immune system could be a potential therapeutic target for HD. AREAS COVERED: To date, the number of trials targeting immune aspects of HD has been limited. However, targeting it, may have great advantages over other therapeutic areas, given that many drugs already exist that have actions in this system coupled to the fact that inflammation can be measured both peripherally and, to some extent, centrally using CSF and PET imaging. In this review, we look at evidence that the immune system and the newly emerging area of the microbiome are altered in HD patients, and then present and discuss clinical trials that have targeted different parts of the immune system. EXPERT OPINION: We then conclude by discussing how this field might develop going forward, focusing on the role of imaging and other biomarkers to monitor central immune activation and response to novel treatments in HD.
Assuntos
Biomarcadores , Doença de Huntington , Inflamação , Doença de Huntington/tratamento farmacológico , Doença de Huntington/fisiopatologia , Doença de Huntington/imunologia , Humanos , Animais , Inflamação/tratamento farmacológico , Inflamação/imunologia , Biomarcadores/metabolismo , Terapia de Alvo Molecular , Progressão da Doença , Desenvolvimento de Medicamentos , Sistema Imunitário/efeitos dos fármacos , MicrobiotaRESUMO
The two-site enzyme immunoassasy (EIA) using the monoclonal antibody (MAb) 27/21 is a valuable method capable of detecting mouse and human NGF quantitatively (Soderstrom et al., 1990). The presence of NGF in serum has been controversial, since t6he previous assay methods failed to detect circulating NGF. Recently, we described the immunological detection of low levels of NGF in human serum samples and introduced a blocking test validating the specificity of the immunoreactivity for NGF in human serum (Lorigados et al., 1982). In the present work, we applied this two-site EIA using monoclonal NGF antibody 27/21 in the study of NGF serum levels from diverse neurodegenerative disorders. We also studied evolutive samples of Parkinson's patients that received neural transplant