Huntington’s disease (HD) is a genetic neurodegenerative disorder that can result in motor, mood and cognitive symptoms. HD pathophysiology has been linked to neuroinflammation, which is the presence of inflammatory mediators and reactive glial cells in the brain parenchyma. Many signalling pathways likely interact to propagate neuroinflammation and contribute to cell loss. Previous literature indicates that in the anterior cingulate cortex, cell loss and neuroinflammation are correlated with HD mood symptoms. This project gives insight into inflammation-related differential gene expression in the HD mid-cingulate cortex (MCC), which has not previously been investigated. We also assessed inflammation-related differential gene expression within different HD symptom presentations, splitting the HD cases in our study into symptom profiles of motor, mood and mixed. We used fourteen HD and nine control post-mortem human MCC samples overall for next-generation mRNA sequencing. These results were anaylsed using Gene Ontology (GO) enrichment analysis and were validated with Nanostring nCounter gene assays. We have found 24 upregulated inflammation-related genes in HD cases overall using mRNA sequencing, including toll-like receptors, classical complement, AQP4, CHI3L1, P2X7R, S100A9 and SPP1. However, 13 inflammation-related markers including chemokines were downregulated. GO enrichment analysis reflected this, with multiple inflammation-related GO terms being upregulated and downregulated in all HD, mood and motor groups. In mood HD cases, 7 inflammation-related genes were upregulated and none were downregulated. These results present a complex picture of potential inflammation priming in the HD MCC, rather than overt neuroinflammation.