Publications by authors named "Ben L Handen"
Article Synopsis
- - This study examines the link between Down syndrome (DS) and early-onset Alzheimer's disease (AD), focusing on how amyloid positivity, memory function, and clinical status change with age.
- - Data from the Alzheimer Biomarker Consortium-Down Syndrome (ABC-DS) was used to analyze amyloid levels and cognitive function in 409 adults with DS, revealing that both amyloid positivity and memory decline increase significantly as individuals age.
- - The research highlights the need for age-specific considerations in monoclonal antibody trials targeting AD in individuals with DS, as there’s a considerable gap between amyloid detection and visible clinical symptoms.
The focus of Alzheimer's disease (AD) neuroimaging research has shifted towards an investigation of the earliest stages of AD pathogenesis, which manifests in every young adult with Down syndrome (DS; trisomy 21) resulting from a deterministic genetic predisposition to amyloid precursor protein overproduction. Due to morphological differences in brain structure in the DS population, special consideration must be given to processing pipelines and the use of normative atlases developed for the non-DS population. Further, the use of typical MRI to MRI template spatial normalization is less desirable in this cohort due to a greater presence of motion artefacts in MRI images.
View Article and Find Full Text PDFBackground: The Down syndrome (DS) population is genetically predisposed to amyloid-β protein precursor overproduction and Alzheimer's disease (AD).
Objective: The temporal ordering and spatial association between amyloid-β, glucose metabolism, and gray matter (GM) volume in the DS population can provide insight into those associations in the more common sporadic AD.
Methods: Twenty-four adults (13 male, 11 female; 39±7 years) with DS underwent [11C]PiB, [18F]FDG, and volumetric MRI scans.
Introduction: Down syndrome (DS) arises from a triplication of chromosome 21, causing overproduction of the amyloid precursor protein and predisposes individuals to early Alzheimer's disease (AD).
Methods: Fifty-two nondemented adults with DS underwent two cycles of carbon 11-labeled Pittsburgh compound B ([C]PiB) and T1 weighted magnetic resonance imaging (MRI) scans 3.0 ± 0.