TMAO, or trimethylamine N-oxide, is a small molecule associated with interactions between gut microbes and the body’s metabolism of dietary compounds. A human study found higher TMAO in the cerebrospinal fluid of people with mild cognitive impairment and Alzheimer’s dementia than in cognitively unimpaired participants. That finding links TMAO to Alzheimer’s-related biomarkers; it does not show that TMAO causes the disease or that lowering it would prevent or treat it.
What is TMAO?
Trimethylamine N-oxide (TMAO) is a molecule associated with the metabolism of choline and other dietary precursors. In a simplified pathway, gut microbes can transform precursor compounds into trimethylamine, which the body then converts into TMAO. Its production therefore involves both microbial and host metabolism; it is not simply a toxin made by one food.
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TMAO has been studied in several disease contexts, but its presence or level alone does not diagnose Alzheimer’s disease.
What did the human Alzheimer’s study find?
A 2018 study measured TMAO in cerebrospinal fluid (CSF), the fluid surrounding the brain and spinal cord, from 410 participants: 40 with Alzheimer’s clinical syndrome, 35 with mild cognitive impairment (MCI), and 335 who were cognitively unimpaired. After adjustment for age, sex, and APOE ε4 genotype, CSF TMAO was higher in the MCI and Alzheimer’s dementia groups than in the cognitively unimpaired group. The study also found associations between TMAO and CSF phosphorylated tau, phosphorylated tau/Aβ42, total tau, and neurofilament light, markers related to Alzheimer’s pathology and neuronal injury. Read the study record on PubMed.
These were biomarker associations observed in a cohort, not evidence that TMAO started the disease. The study does not establish which change came first, whether TMAO contributes causally, or whether reducing TMAO would change symptoms or disease progression.
How strong is the evidence for a link?
| Evidence type | What it can show | What it does not establish |
|---|---|---|
| Human observational biomarker study | In the 2018 cohort, CSF TMAO levels differed by cognitive group and were associated with Alzheimer’s-related and neuronal-injury biomarkers. | Cause and effect, the order of changes, or a benefit from lowering TMAO. |
| Mechanistic and animal research | Provides hypotheses about possible biological pathways and justifies further study of Alzheimer’s-like effects. | That the same mechanisms cause Alzheimer’s in people, or that an intervention works in humans. |
Researchers have proposed that microbial metabolites might influence the brain through gut–brain communication and pathways involving inflammation, vascular or endothelial function, amyloid processing, tau-related pathology, and neuronal injury. Reviews discuss these possibilities, but biological plausibility is not proof of a human cause or treatment. A 2021 review described the TMAO–Alzheimer’s link as “far from definitive.” See the 2021 review on PubMed. The National Institute on Aging also provides an overview of research into the gut microbiome and Alzheimer’s disease: Beyond the brain: The gut microbiome and Alzheimer’s disease.
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Does TMAO cause Alzheimer’s disease?
Current evidence does not answer that question with a yes. The observed association could reflect TMAO contributing to disease processes, a downstream response to them, a marker of another process, or some combination. A CSF association cannot distinguish among these possibilities on its own.
A 2025 review synthesizing 92 peer-reviewed animal, human, and meta-analytic studies published from 2010 through 2025 shows that the topic continues to be investigated across different evidence types. A broad review, however, does not turn mixed or indirect evidence into proof of causation. Read the 2025 review on PubMed Central. A 2024 review also examines proposed TMAO mechanisms and the evidence around Alzheimer’s disease: Read the review on PubMed.
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Can lowering TMAO prevent or treat Alzheimer’s?
The evidence discussed here does not show that a diet change, probiotic, supplement, or other way of lowering TMAO prevents Alzheimer’s, treats it, or improves cognition. Reviews call for larger, longitudinal, and mechanistically informed studies before microbiome-directed interventions can be validated.
The Alzheimer’s Association states: “However, not a single food, beverage, ingredient, vitamin or supplement has been proven to prevent, treat or cure Alzheimer’s disease or to benefit cognitive function or brain health.” It also cautions that supplements do not undergo the same FDA review as prescription drugs and may interact with prescribed medicines. See the Alzheimer’s Association’s guidance on alternative treatments.
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For now, TMAO is a subject of research, not an established Alzheimer’s prevention target. A TMAO test, supplement, or product marketed for Alzheimer’s outcomes should not be treated as a proven way to prevent or manage the disease.
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