# Short-term memory conjunctive binding in subjective cognitive decline: A PET biomarker-based study

**Authors:** M. A. Cecchini, A. Studart-Neto, N. C. Moraes, C. G. Carneiro, A. C. Gomes, C. A. Buchpiguel, S. M. D. Brucki, A. M. Coutinho, R. Nitrini, M. S. Yassuda

PMC · DOI: 10.1007/s00415-026-13640-4 · 2026-01-30

## TL;DR

This study investigates whether a memory test can detect early signs of Alzheimer's disease in people with subjective cognitive decline.

## Contribution

The study evaluates the STMCB test's effectiveness in distinguishing early Alzheimer's from controls using PET biomarkers.

## Key findings

- The STMCB test did not show significant differences between controls and SCD participants.
- The test failed to distinguish amyloid-negative controls from SCD participants with amyloid pathology.
- Binding deficits may appear later in Alzheimer's progression, possibly linked to tau or neurodegeneration.

## Abstract

The Short-Term Memory Conjunctive Binding (STMCB) test assesses the ability to maintain integrated shape-colour associations in memory. It has been applied to detect Alzheimer’s disease (AD) across the continuum, from preclinical stages and subjective cognitive decline (SCD) to dementia. The objective of the present study was to examine whether the STMCB test can differentiate individuals at very early stages of AD from controls. The sample included 67 participants with normal performance on standard neuropsychological tests. Participants were classified as controls or as having SCD based on self-reported memory complaints. Twenty-three controls and 44 individuals with SCD completed the STMCB test. All individuals also underwent a comprehensive neuropsychological evaluation, amyloid ([11C]PIB) and FDG-PET scans. No significant group differences were observed in STMCB test performance between the groups. Furthermore, the STMCB test did not distinguish between amyloid-negative controls and SCD participants with amyloid pathology. These findings suggest that binding deficits may emerge later in the AD continuum, particularly when tau deposition or neurodegeneration is present.

The online version contains supplementary material available at 10.1007/s00415-026-13640-4.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975), subjective cognitive decline (MONDO:0850292), dementia (MONDO:0001627)

## Full-text entities

- **Genes:** SCD (stearoyl-CoA desaturase) [NCBI Gene 6319] {aka FADS5, MSTP008, SCD1, SCDOS, hSCD1}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, SM1 (Schistosoma mansoni, susceptibility/resistance to) [NCBI Gene 7911], APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, PSEN1 (presenilin 1) [NCBI Gene 5663] {aka ACNINV3, AD3, CMD1U, FAD, PS-1, PS1}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}
- **Diseases:** amyloid deposition (MESH:D058225), SCD (MESH:D003072), Depression (MESH:D003866), Binding deficits (MESH:D009461), AD (MESH:D000544), episodic memory impairments (MESH:D008569), amyloid (MESH:C000718787), MCI (MESH:D060825), amyloidosis (MESH:D000686), anxiety (MESH:D001007), AB (MESH:D049290), psychiatric (MESH:D001523), neurodegeneration (MESH:D019636), visual, auditory, or motor impairments (MESH:D014786), major depression (MESH:D003865), cancer (MESH:D009369), Dementia (MESH:D003704)
- **Chemicals:** PIB (MESH:C069442), glucose (MESH:D005947), FDG (MESH:D019788), 11C]PIB (MESH:C475519), carbon-11 (MESH:C000615233), Coutinho (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** E280A

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12858614/full.md

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Source: https://tomesphere.com/paper/PMC12858614