Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 26, Issue -, Pages 33-38Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2015.09.008
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Funding
- Medical Research Council (UK) [MR/L02053X/1]
- NIHR Biomedical Research Centre at University College London Hospitals NHS Foundation Trust and University College London [BRC230/NS/RA/101410]
- UK Dementia and Neurodegenerative Diseases Network (DeNDRoN)
- MRC [MR/L012936/1] Funding Source: UKRI
- Medical Research Council [MR/L012936/1, MR/P007015/1] Funding Source: researchfish
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Innate immune dysfunction is increasingly recognised as a key characteristic of neurodegenerative disease. In the fatal inherited neurological disorder, Huntington's disease, altered innate immune cell function and increased inflammation are observed in the brain and the periphery of disease gene carriers many years before symptom onset, suggesting a potentially early and important role in disease pathogenesis. This is due, at least in part, to the intrinsic effects of the disease-causing protein, mutant huntingtin, expressed in innate immune cells themselves. Understanding whether such innate immune dysfunction in Huntington's disease can be targeted to slow the onset and/or the progression of the disease has significant therapeutic implications and is the subject of much current research.
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