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Alzheimer's Association International Conference 2026

July 12-15, 2026 | London, United Kingdom, and Online

5315

Exploring Causal Links Between Sleep And Cognitive Performance: Evidence From Twin-based Mendelian Randomization

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Poster Presenter

Tina Vo

Authors

Tina Vo-Eckerle, Nathan Gillespie, Luis Castro de Araujo, Ole Andreassen, Tyler Bell, Anders Dale, Richard Hauger, Jack Hunt, Mark Logue, Michael Neale, Olivia Puckett, Rongxiang Tang, Rosemary Toomey, Hong Xian, Christine Fennema-Notestine, Carol Franz, William Kremen, Michael Lyons, Chandra Reynolds, Jeremy Elman, Matthew Panizzon

Affiliations

Department of Psychological and Brain Sciences, Texas A&M University, J. Craig Venter Institute, Department of Psychiatry, University of California, San Diego; Center for Behavior Genetics of Aging, University of California, San Diego, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia, Commonwealth University, Institute of Clinical Medicine, Department of Psychiatry, University of Oslo, Department of Psychiatry, University of Washington, Department of Biomedical Genetics, Boston University Medical Campus, Department of Psychological & Brain Sciences, Boston University, Department of Epidemiology and Biostatistics, St. Louis University, Institute for Behavioral Genetics, University of Colorado Boulder, Department of Psychology and Neuroscience, University of Colorado Boulder

Part of Topic

Exploring Causal Links Between Sleep And Cognitive Performance: Evidence From Twin-based Mendelian Randomization

Poor sleep quality (SQ) is associated with diminished cognitive performance, and both are linked to elevated risk for Alzheimer’s disease and related dementias.1-3

Determining whether these associations are causal is critical for evaluating sleep as a modifiable target for preserving cognitive health and reducing dementia risk.

Participants

Participants included 798 men (230 Monozygotic Twin Pairs, 169 Dizygotic Twin Pairs) from the Vietnam Era Twin Study of Aging (VETSA)4:

Age: M =67.34 years (SD=2.50), Range= 61.37 – 73.25 years

•Sleep Quality: Global Pittsburgh Sleep Quality Index5 Score (PSQI) M= 5.53 (SD=3.73)

•Sleep Duration

•A single component within the PSQI: “During the past month, how many hours of actual sleep did you get at night?” M = 6.80 (SD=1.33)

•Sleep Health PGS, Habitual Sleep Duration PGS, and General Cognitive Ability PGS were used as instrumental variables

•

Instrument strength reflects how well each PGS predicts its target phenotype; stronger instruments improve power to distinguish causal effects from shared genetic liability.

•Sleep Health-PGS moderately predicted SQ

•F(1,957) = 7.17, p < 0.01

•Sleep-Duration-PGS strongly predicted sleep duration

•F(1,957) = 24.57, p < 0.001

•GCA-PGS strongly predicted all six cognitive measures

•F = 14.57–50.96.

•

•General Cognitive Ability (GCA) and domain factor scores: executive function, visual-spatial ability, verbal fluency, episodic memory, and processing speed

Advantages of the MR-DoC2 Method

•MR-DoC2 combines twin-based Direction of Causation (DoC) modeling with Mendelian Randomization (MR).

•Extends traditional MR by accounting for unmeasured genetic and environmental confounding.

•Tests bidirectional causal effects while controlling for shared familial influences.

Evidence for bidirectional causal effects (SQ ↔ Cognition)

•Removing both the SQ → cognition path (g1) and cognition → SQ path (g2) significantly worsened model fits for SQ with:

•GCA: χ²(2) = 6.90, p = 0.03

•Visual-spatial ability: χ²(2) = 7.50, p = 0.02

•Processing speed: χ²(2) = 9.43, p = 0.01

•Best-fitting models generally favored SQ → cognition over cognition → SQ effects for:

•GCA, visual-spatial ability, and processing speed.

•Effect sizes were modest (SQ → cognition: d ≈ −0.18 to −0.26; small effects)

•Modest, potentially bidirectional effects between sleep quality and cognition for GCA, visual-spatial ability, and processing speed.

•No causal associations were observed between sleep duration and cognitive performance.

•Sleep quality—rather than duration—may be a promising target for preserving cognitive functioning, as it is more amenable to intervention.

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