Table 2.

Positron emission tomography imaging studies assessing microglia in Huntington’s disease.

Study	Subjects	PET technique	Main findings
Pavese et al. (2006)	11 manifest HD patients, 10 NC	11C-PK11195	Significantly increased 11C-PK11195 BPND in patients than controls Increased 11C-PK11195 uptake correlated positively with disease severity
Tai et al. (2007)	11 premanifest HD subjects, 10 NC	11C-PK11195	Significantly higher striatal 11C-PK11195 BPND that correlated inversely with D2 receptor availability
			Higher striatal uptake correlated with 5 year probability of clinical disease onset
Politis et al. (2008)	10 premanifest HD subjects, 9 manifest HD patients, 10 NC	11C-PK11195	Significantly increased hypothalamic 11C-PK11195 BPND in both premanifest and manifest subjects compared to controls
			Inverse correlation between increased hypothalamic 11C-PK11195 BPND and D2 receptor availability
Politis et al. (2011)	8 premanifest HD subjects, 8 manifest HD patients, 16 NC	11C-PK11195	In premanifest subjects, increased microglial activation in cognitive regions correlated with 5 year probability of clinical disease onset.
			In manifest HD patients, significantly increased 11C-PK11195 BPND in globus pallidus, anterior prefrontal cortex, and limbic striatum

BP_ND, binding potential; HD, Huntington’s disease; NC, normal control.