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Plasma trimethylamine N-oxide (TMAO): associations with cognition, neuroimaging, and dementia

Abstract:

Background

The gut-derived metabolite Trimethylamine N-oxide (TMAO) and its precursors - betaine, carnitine, choline, and deoxycarnitine – have been associated with an increased risk of cardiovascular disease, but their relation to cognition, neuroimaging markers, and dementia remains uncertain.

Methods

In the population-based Rotterdam Study, we used multivariable regression models to study the associations between plasma TMAO, its precursors, and cognition in 3,143 participants. Subsequently, we examined their link to structural brain MRI markers in 2,047 participants, with a partial validation in the Leiden Longevity Study (n = 318). Among 2,517 participants, we assessed the risk of incident dementia using multivariable Cox proportional hazard models. Following this, we stratified the longitudinal associations by medication use and sex, after which we conducted a sensitivity analysis for individuals with impaired renal function.

Results

Overall, plasma TMAO was not associated with cognition, neuroimaging markers or incident dementia. Instead, higher plasma choline was significantly associated with poor cognition (adjusted mean difference: -0.170 [95% confidence interval (CI) -0.297;-0.043]), brain atrophy and more markers of cerebral small vessel disease, such as white matter hyperintensity volume (0.237 [95% CI: 0.076;0.397]). By contrast, higher carnitine concurred with lower white matter hyperintensity volume (-0.177 [95% CI: -0.343;-0.010]). Only among individuals with impaired renal function, TMAO appeared to increase risk of dementia (hazard ratio (HR): 1.73 [95% CI: 1.16;2.60]). No notable differences were observed in stratified analyses.

Conclusions

Plasma choline, as opposed to TMAO, was found to be associated with cognitive decline, brain atrophy, and markers of cerebral small vessel disease. These findings illustrate the complexity of relationships between TMAO and its precursors, and emphasize the need for concurrent study to elucidate gut-brain mechanisms.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1186/s13195-024-01480-1

Authors


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Role:
Author
ORCID:
0000-0002-3579-8054


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Funder identifier:
https://ror.org/04jsz6e67
Grant:
184.033.111
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Funder identifier:
https://ror.org/00k4n6c32
Grant:
259679


Publisher:
BioMed Central
Journal:
Alzheimer's Research and Therapy More from this journal
Volume:
16
Issue:
1
Article number:
113
Place of publication:
England
Publication date:
2024-05-20
Acceptance date:
2024-05-13
DOI:
EISSN:
1758-9193
Pmid:
38769578


Language:
English
Keywords:
Pubs id:
2000671
Local pid:
pubs:2000671
Deposit date:
2024-07-04

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