AD-Related Pathology and Gray Matter Atrophy Rates in Probable Dementia with Lewy Bodies (P6.232)

Objective: We investigated the longitudinal rates of GM atrophy and their association with baseline Aβ deposition in a cohort of patients with probable dementia with Lewy bodies(DLB). Background: More than 50[percnt] of patients with probable DLB show Amyloid-beta (Aβ) deposition as measured with C11-Pittsburgh-compound-B (PiB) binding on PET. The association of Aβ deposition, as a marker of Alzheimer’s disease (AD) pathology, with structural brain changes in patients with DLB is unknown. Methods: Patients with probable DLB (n=19), who were consecutively recruited to the Mayo Clinic AD Research Center, underwent PiB-PET and MRI examinations at baseline. A second MRI was performed after a mean(SD) follow-up period of 2.5(1.2) years. Regional GM loss was determined on a high resolution 3D-T1 MRI with the Tensor Based Morphometry-Symmetric Normalization. Linear regression was performed between both global and regional baseline PiB standard unit value ratio (SUVR) and longitudinal change in regional GM volumes from an in-house modified anatomic atlas adjusting for age. Results: DLB patients had a mean(SD) PiB SUVR of 1.53(0.36). Higher regional and global PiB SUVR was associated with greater GM loss in the medial temporal lobe, caudate, putamen, posterior cingulate cortex and occipital cortex, after adjusting for age (p=<0.05). Conclusions: In patients with probable DLB, presence of AD-related pathology is associated with GM atrophy rates in the limbic and paralimbic cortex as well the occipital lobe and corpus striatum. We previously showed that autopsy-confirmed DLB patients have increased GM atrophy rates in the limbic and paralimbic cortices only if they have additional AD-related pathology, particularly neurofibrillary tangle pathology. Current data suggest that presence of Aβ deposition is associated with the evolution of neurodegeneration potentially due to AD-related pathology in these regions. In addition, increased rates of atrophy in the corpus striatum may suggest a potential interaction of Aβ deposition with LB disease.