Dementia with Lewy bodies : the investigation of pre- and post-synaptic dopaminergic receptors with SPET

Objective: Dementia with Lewy bodies (DLB) is one of the main differential diagnoses of Alzheimer's disease (AD). Key pathological features of patients with DLB are not only the presence of cerebral cortical neuronal loss, with Lewy bodies in surviving neurones, but also loss of nigrostriatal dopaminergic neurones, similar to that of Parkinson's disease (PD). In vivo detection of this dopaminergic degeneration and post-synaptic dopamine D2 deregulation might help to distinguish DLB from AD during life. Methods: Using a dopaminergic post-synaptic ligand 123I-iodobenzamide (IBZM) and pre-synaptic ligand [123I]-2β-carbometoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (FP-CIT) and single photon emission tomography (SPET) we assessed the integrity of the nigrostriatal metabolism. Results: IBZM study-The DLB group had a significantly lower left caudate:putamen ratio than the control and the AD group. The DLB group also had a lower right caudate:putamen ratio than the AD group and the controls, but the difference between the DLB and AD group was not significant. Results: FP-CIT study - Both DLB and PD patients had significantly lower pre-synaptic radioactivity uptake than AD patients and controls in the caudate nucleus and the anterior and posterior putamen. There was significantly greater asymmetry of uptake in the posterior putamina of PD patients than DLB patients. The mean caudate:putamen ratio for the DLB group was not significantly different to that of the controls, while the mean caudate:putamen ratio for the PD group was significantly higher than for the control group and for the DLB group. Conclusion: Our results show that FP-CIT SPET provides a means of distinguishing DLB from AD during life. There are also clear differences between PD and DLB in the pattern of striatal dopaminergic dysfunction. DLB patients do not have the characteristic selective degeneration of ventrolateral nigral neurons that has been shown in PD. Patients with DLB have also changes in striatal post-synaptic D2 receptors, but these are unlikely to be of value in distinguishing DLB from AD during life.