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J Neuroinflammation ; 20(1): 79, 2023 Mar 21.
Artigo em Inglês | MEDLINE | ID: mdl-36945016

RESUMO

Neuroinflammation has been suggested as a pathogenetic mechanism contributing to Parkinson's disease (PD). However, anti-inflammatory treatment strategies have not yet been established as a therapeutic option for PD patients. We have used a human α-synuclein mouse model of progressive PD to examine the anti-inflammatory and neuroprotective effects of inflammasome inhibition on dopaminergic (DA) neurons in the substantia nigra (SN). As the NLRP3 (NOD-, LRR- and pyrin domain-containing 3)-inflammasome is a core interface for both adaptive and innate inflammation and is also highly druggable, we investigated the implications of its inhibition. Repeat administration of MCC950, an inhibitor of NLRP3, in a PD model with ongoing pathology reduced CD4+ and CD8+ T cell infiltration into the SN. Furthermore, the anti-inflammasome treatment mitigated microglial activation and modified the aggregation of α-synuclein protein in DA neurons. MCC950-treated mice showed significantly less neurodegeneration of DA neurons and a reduction in PD-related motor behavior. In summary, early inflammasome inhibition can reduce neuroinflammation and prevent DA cell death in an α-synuclein mouse model for progressive PD.


Assuntos
Inflamassomos , Doença de Parkinson , Humanos , Camundongos , Animais , Inflamassomos/metabolismo , Doença de Parkinson/tratamento farmacológico , Doença de Parkinson/etiologia , Doença de Parkinson/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , alfa-Sinucleína/metabolismo , Neurônios Dopaminérgicos , Doenças Neuroinflamatórias , Microglia/metabolismo , Camundongos Endogâmicos NOD , Sulfonamidas/farmacologia , Modelos Animais de Doenças , Camundongos Endogâmicos C57BL
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