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Alzheimer's Association International Conference 2026

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

1002

Causal Inference Analysis Of The Effect Of Beta-amyloid And Tau Proteins On Dementia Risk: A Mendelian Randomization Analysis

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Poster Presenter

Jacob Ayembilla

Authors

Jacob Apibilla Ayembilla, Rachael Osemudiamen Osagie, Adeyemi Timothy Akinade, Oumar Sako, Oluwafunmbi Ebenezer Ogunmiluyi, Olaitan I. Awe

Affiliations

Department of Science Laboratory Technology, Accra Technical University, Accra, Ghana., Faculty of Dental Medicine and Oral Health Sciences, McGill University, Montreal, QC, Canada., Department of Genetics and Biochemistry, Clemson University, South Carolina, SC, USA., African Centre of Excellence in Bioinformatics and Data Intensive Science (ACE-B), University of Sciences Techniques and Technologies of Bamako, Bamako, Mali., Department of Physiology, University of Medical Sciences, Ondo, Ondo State, Nigeria., Department of Computer Science, University of Ibadan,, Ibadan, Oyo State, Nigeria.

Part of Topic

Video

Causal inference analysis of the effect of β-amyloid and tau proteins on dementia risk: A Mendelian randomization analysis.

Jacob Apibilla Ayembilla1, Rachael Osemudiamen Osagie2, Adeyemi Timothy Akinade3, Oumar Sako4, Oluwafunmbi Ebenezer Ogunmiluyi5, Olaitan I. Awe6.

1Department of Science Laboratory Technology, Accra Technical University, Accra, Ghana, 2Faculty of Dental Medicine and Oral Health Sciences, McGill University, Montreal, QC, Canada, 3Department of Genetics and Biochemistry, Clemson University, South Carolina, SC, USA, 4African Centre of Excellence in Bioinformatics and Data Intensive Science (ACE-B), University of Sciences Techniques and Technologies of Bamako, Bamako, Mali, 5Department of Physiology, University of Medical Sciences, Ondo, Ondo State, Nigeria, 6Department of Computer Science, University of Ibadan,, Ibadan, Oyo State, Nigeria.

Study Highlights

1. CSF phosphorylated tau (p-tau) appears to play a causal role in Alzheimer's disease and vascular dementia.

2. Amyloid-β and tau exhibit distinct effects across dementia subtypes.

3. Biomarker-specific pathways may improve dementia risk stratification and precision medicine.

Introduction

�� Dementia is a growing global health challenge

•Dementia affects more than 55 million people worldwide, with numbers expected to increase substantially due to population ageing.

•Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VaD) are among the most common dementia subtypes.

•Effective disease-modifying therapies remain limited, highlighting the need to identify causal biological mechanisms.

�� What is missing in current knowledge

•Amyloid-β (Aβ), tau, and phosphorylated tau (p-tau) are established biomarkers of neurodegeneration and are widely used in diagnosis and research.

•However, it remains unclear whether these biomarkers are causally involved in dementia pathogenesis or are simply consequences of disease progression.

•Most evidence comes from observational studies, which are vulnerable to confounding and reverse causation.

•The causal effects of CSF and plasma Aβ, tau, and p-tau across different dementia subtypes remain poorly understood.

�� Why this study is important

•Uses Mendelian randomization (MR) to strengthen causal inference between biomarkers and dementia risk.

•Examines both CSF and plasma biomarkers, providing insights into central and peripheral pathological processes.

•Investigates causal effects across multiple dementia subtypes (AD, FTD, and VaD) rather than focusing on AD alone.

•Identifies biomarker-specific pathways that may improve risk stratification, early detection, and therapeutic target prioritization.

•Provides evidence for precision medicine approaches in dementia prevention and treatment

Aim

To determine whether genetically predicted amyloid-β, tau, and phosphorylated tau levels causally influence the risk of AD, FTD, and VaD.

Conclusion

•CSF phosphorylated tau (p-tau) shows a likely causal role in Alzheimer’s disease and vascular dementia, supporting tau pathology as a key disease driver.

•Amyloid-β and tau biomarkers demonstrate differential causal effects across dementia subtypes, indicating distinct underlying disease mechanisms for AD, FTD, and VaD.

•Elevated plasma Aβ42 may be protective against FTD, while CSF amyloid and tau effects vary by context and model.

•Findings support the use of genetically informed evidence (Mendelian randomization) to clarify biomarker causality beyond observational associations.

•Results highlight the potential for biomarker-guided risk stratification and targeted therapeutic strategies across dementia subtypes.

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