These findings identify TREM2 and TLR4 as potential genetic modifiers for HD and suggest that inflammation influences disease progression in this condition.
<b>Areas covered</b>: We considered available evidence implicating TLR 4 activation in the following CNS pathologies: Alzheimer's disease, Parkinson's disease, ischemic stroke, traumatic brain injury, multiple sclerosis, multiple systems atrophy, and Huntington's disease.
sTLR4 correlates with inflammatory and nutritional parameters, presenting as a new potential player in modulating subclinical inflammation in HD patients.
Cathelicidin, TNF-α, IL-6, IL-10 and MCP-1 were analyzed via ELISA.TLR4 expression in neutrophils was higher in HD patients than in stage 3 and 4 CKD patients.