Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

Abstract

Background: In addition to Lewy body pathology, amyloid-β plaques and neurofibrillary tangles that are characteristic for Alzheimer’s disease (AD) are also frequently found in Lewy body diseases (LBD). We investigate tau accumulation patterns in dementia with Lewy bodies (DLB) and other LBDs using in vivo 18F-AV-1451 positron emission tomography (PET). Methods: We included 12 Parkinson’s disease with normal cognition (PDNC), 22 Parkinson’s disease with cognitive impairment (PDCI), and 18 DLB patients. In addition, 25 AD patients and 25 healthy controls were included for comparison. All participants underwent 18F-AV-1451 and 18F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. Results: Compared to the controls, DLB patients showed slightly increased 18F-AV-1451 binding in the primary sensorimotor and visual cortices as well as the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive DLB patients showed significantly increased binding in the same regions compared to controls, and even greater binding in the primary sensorimotor and visual cortices than AD. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in AD. In DLB, 18F-AV-1451 binding in the occipital cortex correlated with 18F-florbetaben binding. Amyloidnegative PDNC, PDCI and DLB patients did not show increased 18F-AV-1451 binding. Conclusions: DLB patients may harbor 18F-AV-1451 binding patterns distinct from AD, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases within the LBD spectrum, and amyloid may play an important role in the accumulation of neocortical tau in LBD.