. Relationship of neuropathological markers of white matter burden and amyloid accumulation to attentional control during aging. Human Amyloid Imaging 2011 Meeting Abstracts. 2011 Jan 15;

Abstract:

Apparently healthy older adults often harbor various neuropathologies, including white matter burden and amyloidbeta accumulation. White matter abnormalities have been previously associated with declines in executive function, whereas amyloid accumulation has been associated with disruption of memory-related systems. We investigated disruption of executive function operationally defined as failures to dynamically allocate attention across levels of task difficulty during a functional magnetic resonance imaging (fMRI) task. The task involved parametric manipulations of task demand in a global-local paradigm by varying the invocation of inhibition and shifting requirements. Fifty-one younger (aged 18-27) and 62 older adults (aged 60-87) participated in the globallocal task paradigm while undergoing fMRI scanning. All older adults were cognitively normal individuals with a Clinical Dementia Rating of 0. Older adults displayed a pattern of greater activation than younger adults in frontal and parietal regions associated with attentional control. However, older adults who exhibited a pattern of increasing activation as task demand increased also exhibited better performance than did older adults who exhibited a failure to dynamically modulate activation across task difficulty levels. Among older adults with high white matter burden measured from hyperintensities in fluid attenuation inversion recovery (FLAIR) images, there was a significant correlation between white matter burden and the tendency to exhibit failures to dynamically allocate attention. In contrast, an individualfs level of amyloid accumulation as measured with Pittsburgh Compound B using positron emission tomography (PET) was not related to dynamic allocation of attention. Among this cognitively normal sample of older adults, there was little co-occurrence of white matter burden and amyloid accumulation, further suggesting that these two neuropathological markers have distinct etiologies and effects on neural function.

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