From cognition to molecules: tracking brain amyloid-β with memory markers for Alzheimer’s disease

Mario Alfredo Parra, Yunglin Gazes, Yaakov Stern

Research output: Contribution to journalConference Contribution


Background: Short-term memory binding (STMB) declines in asymptomatic carriers of PSEN1 mutations who inevitably develop Alzheimer’s disease (AD). Such subtle memory impairments, which are also found in older adults with subjective cognitive decline (SCD), stand out from a completely normal neuropsychological background. Whether they result from the early brain accumulation of molecules involved in the AD pathology is still unknown. The present study investigated such an association in still healthy older adults. Methods:A sample of 39 healthy older adults was assessed with the STMB test and traditional neuropsychological tasks. The STMB test required participants to detect (i.e., recognize) changes in shapes, colors (baseline conditions), or in shape-color combinations (the binding condition) across two sequential arrays. Participants also underwent Amyloid PET imaging using 18F-Florbetaben. Using previously reported cut-off scores, participants were classified as amyloid negative and positive. Behavioral and neuroimaging variables were compared across groups. Results:We found that 46% of the sample fell below cut-off only on the binding condition of the STMB test. Baseline performance did not differ across groups. This yielded the Group x Condition interaction previously reported in asymptomatic and early prodromal cases (Figure 1A). Neuroimaging analysis of PET data revealed that, relative to Strong Binders, Weak Binders had a significant increase of amyloid-b in brain areas known to be STMB hubs (i.e., parietal-occipito-temporal regions and fusiform gyrus) (Figure 1B). Of note, Strong and Weak Binders could not be distinguished based on performance on traditional neuropsychological tasks. Conclusions:STMB deficits found in otherwise asymptomatic older adults are linked to early accumulation of amyloid-b. Such an association was paramount in brain regions known to be part of the sub-hippocampal network which is thought of as the seat of the earliest pathological changes of AD. Future studies should investigate if healthy older adults whose STMB abilities are hampered by increased amyloid-b deposits are those who are already embarked on the continuum of AD.
Original languageEnglish
Pages (from-to)P692-P692
Number of pages1
JournalAlzheimer's and Dementia
Issue number7S Part 14
Publication statusPublished - 1 Jul 2017
EventAlzheimer's Association International Conference 2017 - London, United Kingdom
Duration: 16 Jul 201720 Jul 2017


  • short-term memory binding
  • Alzheimer's disease
  • memory impairments

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