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. Author manuscript; available in PMC: 2019 Sep 20.
Published in final edited form as: Int Rev Neurobiol. 2018 Sep 20;141:211–250. doi: 10.1016/bs.irn.2018.07.027

Table 4.

Summary of nAChR SPECT and PET binding studies in PD and parkinsonian dementia.

Reference nAChR ligand Population Main findings and clinical correlates
(Fujita et al., 2006). [123I]-5-IA-85380 PD Widespread cortical and subcortical nAChR binding reductions in the PD patients compared to control subjects, including the pons, cerebellum, striatum and thalamus.
(Oishi et al., 2007) [123I]-5-IA-85380 PD Widespread cortical and subcortical nAChR binding reductions in PD patients compared to control subjects, in particular in the frontal cortex and brainstem.
(Meyer et al., 2009) [18F]-Fluoro-A-85380 PD Widespread cortical and subcortical losses, including the hippocampus, amygdala, cerebellum, thalamus, and putamen in PD patients compared to control subjects.
(Kas et al., 2009) [18I]-Fluoro-A-85380 PD Reduced nAChR binding in the substantia nigra and the striatum in the PD patients compared to the normal control subjects.
(O’Brien et al., 2008) [123I]-5-IA-85380 DLB Reduced nAChR binding in striatal, left superior temporal, right inferior frontal and cingulate gyri regions except for relatively increased occipital (bilateral cuneus) and left precuneus receptor binding.
(Colloby et al., 2010) [123I]-5-IA-85380 DLB Decreased nAChR binding in left superior, middle, and inferior frontal gyri and pre-/post-central and anterior cingulate regions significantly correlated with decline in executive function in a pooled analysis comprising DLB and AD patients.