Abstract
Introduction18F-florbetaben and positron emission tomography were used to examine the relationships between β-amyloid (Aβ) deposition, cognition, hippocampal volume, and white matter hyperintensities in mild cognitive impairment (MCI).MethodsForty-five MCI participants were evaluated. A neocortical standardized uptake value ratio threshold ≥ 1.45 was used to discriminate high from low Aβ burden. Correlations were adjusted for age, gender and years of education.ResultsHigh Aβ burden was found in 53% of MCI. Regression analyses showed standardized uptake value ratio (r = -0.51, P = 0.0015) and hippocampal volume (r = 0.60, P = 0.024) both contributing to episodic memory impairment in independent fashion. White matter hyperintensities correlated with nonmemory cognition, and this correlation was particularly associated with Aβ burden.ConclusionHigher Aβ deposition in MCI is associated with more severe memory impairment and is contributing to early amnestic symptoms independent of hippocampal atrophy.
Highlights
18F-florbetaben and positron emission tomography were used to examine the relationships between b-amyloid (Ab) deposition, cognition, hippocampal volume, and white matter hyperintensities in mild cognitive impairment (MCI)
Twenty-nine participants were classified as having amnestic multidomain mild cognitive impairment (amMCI) and 12 were assessed as having amnestic single-domain mild cognitive impairment (asMCI)
The observation that 53% of scans had high FBB retention is consistent with the prevalence of Alzheimer’s disease (AD) neuropathology at postmortem in those with MCI or in those who progress from MCI to dementia [39,40] and with reports that have used Pittsburgh Compound B (PiB) positron emission tomography (PET) or cerebrospinal fluid measures to assess brain Ab in MCI [41,42,43]
Summary
18F-florbetaben and positron emission tomography were used to examine the relationships between b-amyloid (Ab) deposition, cognition, hippocampal volume, and white matter hyperintensities in mild cognitive impairment (MCI). The leading etiological hypothesis of Alzheimer’s disease (AD) points to excessive brain b-amyloid (Ab) that aggregates to form extracellular plaques and vascular wall deposits [1]. Dementia is usually preceded by a transition period of cognitive decline commonly referred to as mild cognitive impairment (MCI). Characterized by an objective impairment of memory and/or other cognitive domains, MCI is not severe enough to significantly interfere with activities of daily living [2]. The prevalence of MCI in people aged 65 is believed to be 10 to 20%, with over 10% who have been classified as MCI converting to dementia per year [3]. Histopathologic studies on brains of MCI subjects
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