Early microglial activation and peripheral inflammation in dementia with Lewy bodies.

摘要: Inflammation is increasingly recognized as part of the pathology neurodegenerative conditions such Alzheimer's disease and Parkinson's disease, but its role in dementia with Lewy bodies remains unclear. Using multimodal imaging peripheral cytokine analysis, we therefore investigated central inflammation this common form dementia. Nineteen participants probable 16 similarly aged controls underwent 3 T MRI PET 11C-PK11195, a marker microglial activation vivo. Peripheral blood inflammatory cytokines were also measured all subjects, well an additional 10 controls, using Mesoscale Human Cytokine 36 plex panel assays for high sensitivity c-reactive protein, tumour necrosis factor receptor 1, IL-34, YKL-40 (chitinase-3-like protein 1) colony stimulating 1. To test presence vivo amyloid, 11C-Pittsburgh compound B was performed body participants. Microglial elevated subjects mild when compared to those moderate/severe impairment, where severity indexed by cognitive performance on revised Addenbrooke's Cognitive Examination. In patients, strong correlations found between 11C-PK11195 non-displaceable binding potential several regions including caudate nucleus (R = 0.83, P 0.00008) cuneus 0.77, 0.0005). Several altered patients macrophage protein-3 (P 0.001), IL-17A 0.008) IL-2 0.046) reduced IL-8 0.024). There no correlation cortical standardized uptake value ratio clinical features, regional or levels. Nor there any potentials ratios. Our findings provide evidence both changes bodies, occurring early key known be associated pathology, before declining cognition declines. Raised cell function further suggest adaptive immune system pathogenesis disease.