MULTIMODALITY IMAGING FOR EARLY DIAGNOSIS OF DEMENTIA WITH LEWY BODIES

Abstract

The differential diagnosis of patients with Alzheimer's disease (AD) dementia and dementia with Lewy bodies (DLB) is challenging, because the underlying pathology is frequently complex with contribution from both AD and Lewy body disease pathologies. The potential for disease-modifying treatments for AD dementia, as well as the responsiveness to cholinesterase inhibitor treatment and marked neuroleptic sensitivity of DLB patients generate the need for surrogate markers for AD and Lewy body disease pathologies early in the course in DLB. Multimodality imaging provides complementary information on the contribution of AD and Lewy body disease pathologies in patients with DLB. Mild cognitive impairment (MCI) patients with non-amnestic features, especially those with REM sleep behavior disorder (RBD) progress more frequently to DLB than AD, however many MCI patients at risk for DLB also have additional AD pathology. Multimodality imaging in MCI patients with non-amnestic features and/or RBD was investigated. We Identified patients with MCI with non-amnestic features and/or RBD (MCI-DLB/AD) who underwent MRI, FDG PET, amyloid PET and DaTScan studies. The association of hippocampal volumes, amyloid load, DLB signature on FDG PET (cingulate island sign) and DaTScan with RBD and memory function in MCI was tested. Imaging findings associated with AD such as hippocampal atrophy and amyloid load on PET is associated with memory impairment in MCI-DLB/AD. On the contrary, patients with MCI-DLB/AD who have RBD have less hippocampal atrophy and amyloid load than those who do not have RBD, but they are more likely to have the DLB signature on FDG PET (cingulate island sign) and an abnormal DaTScan. Imaging markers of Lewy body disease and AD may provide complementary information in characterizing the underlying pathologies and their contribution to cognitive impairment in patients with MCI who are at an increased risk for DLB. Determining the contribution of Lewy body disease and AD pathologies to MCI would have important implications for secondary prevention of dementia in these individuals.