ArticleBrain and behavior2026
Evaluating the 8-Year Association Between Cognition and Beta Amyloid in the Dallas Lifespan Brain Study Cohort.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Evaluating the 8-Year Association Between Cognition and Beta Amyloid in the Dallas Lifespan Brain Study Cohort.Brain and behavior · 2026Article
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5 authors.
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Abstract
backgroundMounting evidence suggests beta amyloid (Aβ) is not the sole initiating driver of cognitive decline in Alzheimer's disease (AD). This study explores whether there is an association between cognitive decline over eight years and Aβ.
methodsData from 48 participants in the Dallas Lifespan Brain Study (DLBS) were analyzed in the present study. Prior to selection, participants were classified as Aβ
resultsAn association between cognitive decline over 8 years and the Aβ group was observed in reasoning but not across episodic memory, working memory, and processing speed. Still, there were differences between the two groups that reached significance on an episodic memory task (p = 0.035) and trended toward significance on an encompassing episodic memory composite (p = 0.057). Post-hoc comparisons revealed these differences were only significant at epoch 1. Broad declines in cognition were also found over the observation period, irrespective of Aβ group.
conclusionOur results contribute to the mounting evidence that suggests Aβ is not the sole initiating driver of cognitive decline in AD. However, the present study has limitations, including a relatively small sample size that must be accounted for when considering the null findings to prevent overinterpretation. Future work should validate our results in larger, similarly controlled samples and model additional AD biomarkers and risk factors to explore different mechanisms for cognitive decline in AD.
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