Delineating the topography of amyloid-associated cortical atrophy in Down syndrome.

Older adults with Down syndrome (DS) often have Alzheimer's disease (AD) neuropathologies. Although positron emission tomography imaging studies of amyloid deposition (beta amyloid, Aβ) have been associated with worse clinical prognosis and cognitive impairment, their relationships with cortical thickness remain unclear in people with DS. In a sample of 44 DS adults who underwent cognitive assessments, [11C]-PiB positron emission tomography, and T1-weighted magnetization-prepared rapid gradient echo, we used mixed effect models to evaluate the spatial relationships between Aβ binding with patterns of cortical thickness. Partial Spearman correlations were used to delineate the topography of local Aβ-associated cortical thinning. [11C]-PiB nondisplaceable binding potential was negatively associated with decreased cortical thickness. Locally, regional [11C]-PiB retention was negatively correlated with cortical thickness in widespread cortices, predominantly in temporoparietal regions. Contrary to the prevailing evidence in established AD, we propose that our findings implicate Aβ in spatial patterns of atrophy that recapitulated the "cortical signature" of neurodegeneration in AD, conferring support to recent recommendations for earlier disease-interventions. • In a sample of adults with Down''s Syndrome (DS), amyloid burden (Aβ) was strongly associated with cortical thinning. • The topography of Aβ-associated atrophy is similar to the cortical signature of atrophy in Alzheimer's disease. • These findings further implicate Aβ in the pathophysiology of DS. • Further longitudinal studies are necessary to clarify the extent to which baseline Aβ imaging could predict downstream severity of brain atrophy in DS. [ABSTRACT FROM AUTHOR]