Person:
Hanseeuw, Bernard

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Hanseeuw

First Name

Bernard

Name

Hanseeuw, Bernard
Author's Publications: search.filters.isAuthorOfPublication.ec2382b7-9685-499c-ab3f-0b87f658a7a7

Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    The relationship between recall of recently versus remotely encoded famous faces and amyloidosis in clinically normal older adults
    (Elsevier, 2017) Orlovsky, Irina; Huijbers, Willem; Hanseeuw, Bernard; Mormino, Elizabeth C.; Hedden, Trey; Buckley, Rachel; LaPoint, Molly; Rabin, Jennifer; Rentz, Dorene; Johnson, Keith; Sperling, Reisa; Papp, Kathryn
    Introduction: Alzheimer's disease (AD) patients exhibit temporally graded memory loss with remote memories remaining more intact than recent memories. It is unclear whether this temporal pattern is observable in clinically normal adults with amyloid pathology (i.e. preclinical AD). Methods: Participants were asked to recall the names of famous figures most prominent recently (famous after 1990) and remotely (famous from 1960–1980) and were provided with a phonemic cue to ensure that memory failure was not purely due to verbal retrieval weaknesses. In addition, participants identified line drawings of objects. Clinically normal older adults (n = 125) were identified as amyloid β positive or negative (Aβ+/−) using Pittsburgh compound B positron emission tomography. The relationship between Aβ+/− and recall of remote and recent famous face-names and objects was examined using repeated measures analyses and general linear models controlling for demographics and media usage. Results: When provided with a phonemic cue, Aβ+ participants recalled the names of fewer recent famous faces compared with Aβ− participants. However, recall of remote famous face-names and objects did not differ by Aβ group. Discussion Relative sparing of remotely learned information compared with recently learned information is (1) detectable in the preclinical stages of AD and (2) related to amyloid pathology. Both this temporal gradient and assessment of person-centered rather than object-centered semantic information may be particularly meaningful for tracking early memory changes in the AD trajectory.
  • Thumbnail Image
    Publication
    Anosognosia for memory deficits in mild cognitive impairment: Insight into the neural mechanism using functional and molecular imaging
    (Elsevier, 2017) Vannini, Patrizia; Hanseeuw, Bernard; Munro, Catherine E.; Amariglio, Rebecca; Marshall, Gad; Rentz, Dorene; Pascual-Leone, Alvaro; Johnson, Keith; Sperling, Reisa
    Anosognosia, or loss of insight of memory deficits, is a common and striking symptom in Alzheimer's disease (AD). Previous findings in AD dementia patients suggest that anosognosia is due to both functional metabolic changes within cortical midline structures involved in self-referential processes, as well as functional disconnection between these regions. The present study aims to extend these findings by investigating the neural correlates of anosognosia in the prodromal stage of AD. Here, we used regional brain metabolism (resting state 18-F fluorodeoxyglucose positron emission tomography (FDG-PET)) to unravel the metabolic correlates of anosognosia in subjects with amnestic mild cognitive impairment (aMCI) and subsequently resting state functional magnetic resonance imaging (rs-fMRI) to investigate the intrinsic connectivity disruption between brain regions. Thirty-one subjects (mean age: 74.1; Clinical Dementia Rating (CDR) global score: 0.5) with aMCI, and 251 cognitively normal (CN) older adults (mean age: 73.3; CDR: 0) were included as a reference group for behavioral and FDG data. An anosognosia index was obtained by calculating a discrepancy score between subjective and objective memory scores. All subjects underwent FDG-PET for glucose metabolism measurement, and aMCI subjects underwent additional rs-fMRI for intrinsic connectivity measurement. Voxel-wise correlations between anosognosia and neuroimaging data were conducted in the aMCI subjects. Subjects with aMCI had significantly decreased memory awareness as compared to the CN older adults. Greater anosognosia in aMCI subjects was associated with reduced glucose metabolism in the posterior cingulate (PCC) cortices and hippocampus. Intrinsic connectivity analyses revealed a significant association between anosognosia and attenuated functional connectivity between the PCC seed region and orbitofrontal cortex (OFC) as well as bilateral inferior parietal lobes (IPL). These findings provide further evidence that implicates cortical midline structures and hippocampus in the awareness of memory deficits. Investigating neuroimaging changes that co-vary with memory awareness may improve our ability to identify the cause of anosognosia and ultimately increase our chances for its treatment.
  • Thumbnail Image
    Publication
    Interactive versus additive relationships between regional cortical thinning and amyloid burden in predicting clinical decline in mild AD and MCI individuals
    (Elsevier, 2017) d'Oleire Uquillas, Federico; Jacobs, Heidi I.L.; Hanseeuw, Bernard; Marshall, Gad; Properzi, Michael; Schultz, Aaron; LaPoint, Molly R.; Johnson, Keith; Sperling, Reisa; Vannini, Patrizia
    The biological mechanisms that link Beta-amyloid (Aβ) plaque deposition, neurodegeneration, and clinical decline in Alzheimer's disease (AD) dementia, have not been completely elucidated. Here we studied whether amyloid accumulation and neurodegeneration, independently or interactively, predict clinical decline over time in a group of memory impaired older individuals [diagnosed with either amnestic mild cognitive impairment (MCI), or mild AD dementia]. We found that baseline Aβ-associated cortical thinning across clusters encompassing lateral and medial temporal and parietal cortices was related to higher baseline Clinical Dementia Rating Sum-of-Boxes (CDR-SB). Baseline Aβ-associated cortical thinning also predicted CDR-SB over time. Notably, the association between CDR-SB change and cortical thickness values from the right lateral temporo-parietal cortex and right precuneus was driven by individuals with high Aβ burden. In contrast, the association between cortical thickness in the medial temporal lobe (MTL) and clinical decline was similar for individuals with high or low Aβ burden. Furthermore, amyloid pathology was a stronger predictor for clinical decline than MTL thickness. While this study validates previous findings relating AD biomarkers of neurodegeneration to clinical impairment, here we show that regions outside the MTL may be more vulnerable and specific to AD dementia. Additionally, excluding mild AD individuals revealed that these relationships remained, suggesting that lower cortical thickness values in specific regions, vulnerable to amyloid pathology, predict clinical decline already at the prodromal stage.