ArticleDementia and neurocognitive disorders2025
Mendelian Randomization Reveals Unidirectional Links Between Amyloid-β and Tau in Alzheimer's Disease.
Article in Dementia and neurocognitive disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and Purpose: Prior research has indicated that changes in the amyloid-beta (Aβ) biomarker precede tau biomarker alterations in Alzheimer's disease (AD). However, establishing causality through temporal correlations remains contentious. This study aimed to explore the causal relationship between Aβ and tau using Mendelian randomization (MR) analysis. Methods: We conducted two-sample MR analyses employing genome-wide association studies (GWASs) summary statistics for Aβ positron emission tomography (PET) and cerebrospinal fluid phosphorylated tau (CSF pTau). Additionally, to reinforce and validate the results of the two-sample MR, we performed two-sample MR using tau PET GWAS summary statistics and one-sample MR analysis using autopsy data. In the one-sample MR analysis, the exposure and outcome variables were neuritic plaque burden and neurofibrillary tangle burden, respectively, determined through neuropathological examination. Results: The two-sample MR analysis unveiled a causal association between Aβ accumulation and CSF pTau level (BETA [standard error]=0.30 [0.10], Conclusions: Our findings suggest a causal relationship between Aβ burdens and tau burdens in AD, reinforcing the notion of Aβ as a pivotal upstream factor in AD pathogenesis.
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