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

Natalia P. Rocha, Fabiola M. Ribeiro, Erin Furr-Stimming, Antonio L. Teixeira

Research output: Contribution to journalReview articlepeer-review

72 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article number8653132
JournalMediators of Inflammation
Volume2016
DOIs
StatePublished - 2016
Externally publishedYes

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Neuroimmunology of Huntington's Disease: Revisiting Evidence from Human Studies'. Together they form a unique fingerprint.

Cite this