Neuroimmunology of Huntington’s Disease: Revisiting Evidence from Human Studies

Mediators of Inflammation - Tập 2016 - Trang 1-10 - 2016
Natália Pessoa Rocha1, Fabíola M. Ribeiro2, Erin Furr‐Stimming3, Antônio Lúcio Teixeira1
1Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA
2Department of Biochemistry and Immunology, ICB, Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, MG, Brazil
3Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, 77030, USA

Tóm tắt

Huntington’s disease (HD) is a neurodegenerative disorder characterized by selective loss of neurons in the striatum and cortex, which leads to progressive motor dysfunction, cognitive decline, and psychiatric disorders. Although the cause of HD is well described—HD is a genetic disorder caused by a trinucleotide (CAG) repeat expansion in the gene encoding for huntingtin (HTT) on chromosome 4p16.3—the ultimate cause of neuronal death is still uncertain. Apart from impairment in systems for handling abnormal proteins, other metabolic pathways and mechanisms might contribute to neurodegeneration and progression of HD. Among these, inflammation seems to play a role in HD pathogenesis. The current review summarizes the available evidence about immune and/or inflammatory changes in HD. HD is associated with increased inflammatory mediators in both the central nervous system and periphery. Accordingly, there have been some attempts to slow HD progression targeting the immune system.

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