High levels of heart damage biomarker may signal increased dementia risk.
Recent research suggests that higher levels of certain heart-damage biomarkers may signal an increased risk of developing dementia later in life. I’ll walk you through what has been found, what it might mean, and what we don’t yet know. A large long-term study found that people aged approximately 45-69 who had higher mid-life levels of the cardiac biomarker High‑sensitivity cardiac troponin I (hs-troponin I), which signals subtle heart muscle injury, had a significantly higher risk of being diagnosed with dementia decades later.
Specifically, those with the highest troponin levels had about a 38% higher risk of dementia compared with the lowest troponin group. The elevated troponin levels showed up 7 to 25 years before the dementia diagnosis. In a subset of participants with brain MRI, higher troponin levels were associated with smaller hippocampal volume and less grey matter brain changes consistent with aging/degeneration.
More broadly, a review article notes that several cardiac biomarkers, including troponins, N‑terminal pro B‑type natriuretic peptide (NT-proBNP, a marker of cardiac/ventricular stress), and Growth‑differentiation factor 15 (GDF15, a marker of vascular stress), are associated with cognitive impairment or brain changes even in people without overt heart disease. A meta-analysis of coronary heart disease (CHD) found that people with CHD have a higher odds (~1.45 times) of developing cognitive impairment or dementia compared to those without CHD.
What it might mean — possible mechanisms
Here are some ways in which subtle heart damage / cardiovascular dysfunction might contribute to brain aging and dementia risk:
Reduced cerebral perfusion / heart-brain blood flow link: If the heart muscle is damaged (even subtly), cardiac output or the efficiency of circulation might decline, which could impair blood flow to the brain over the years. The brain is highly sensitive to its blood supply.
Vascular damage and micro-injuries: Biomarkers of cardiac injury or stress also correlate with vascular stress. This may manifest in the brain as white matter changes, microinfarcts, or reduced brain tissue volume (as found in the MRI subset).
Shared risk factors: Many heart injury markers are elevated in the presence of high blood pressure, diabetes, high cholesterol, obesity, smoking, etc. These risk factors also contribute to dementia. So part of the association may be explained by overlapping risk pathways.
Early warning / silent damage: The troponin elevations in the study were associated with “subclinical” heart damage (i.e., no overt symptomatic heart disease at baseline). That suggests damage begins much earlier than clinical diagnoses and may set the stage for brain aging for decades.
What we don’t yet caution:
These findings are observational in nature. That means we can’t yet say the elevated troponin caused the dementia, only that there’s an association. Indeed, the Mendelian-randomisation study found little evidence for a causal effect of genetically elevated cardiac biomarkers on dementia risk.
Exactly what threshold of troponin (or other biomarkers) is meaningful, and at what ages, is not yet firmly established. While plausible pathways exist (blood flow, microvascular injury, overlap of cardiovascular & cerebrovascular disease), the precise chain of events linking heart damage → brain injury → dementia remains under investigation.
Many of the studies focus on specific cohorts (e.g., the Whitehall II Study in the UK) and mostly middle-aged adults initially without heart disease. Whether the same associations hold in other populations, ethnicities, or older age groups is still being defined. If elevated cardiac biomarker levels identify a higher risk of dementia, we don’t yet have solid evidence that intervening specifically based on these biomarker levels (e.g., in addition to standard cardiovascular care) will reduce dementia risk.
Implications for health & prevention:
Mid-life heart health appears increasingly important for brain health in later life. What happens to the heart, vessels, and circulation may matter for the brain decades later. Monitoring cardiovascular risk factors (blood pressure, lipids, diabetes, smoking, obesity, physical activity) remains very important because these are modifiable and already known to influence dementia risk.
The idea of using cardiac biomarkers (like troponin) as part of a dementia risk assessment is emerging but not yet ready for routine clinical use solely for that purpose. For individuals, focusing on good cardiovascular health is also brain-health care. Eat healthy, exercise, manage weight/diabetes/hypertension, avoid smoking, and keep cholesterol/lipids in check. For clinicians/researchers: These findings may guide future work on early identification of who is at risk, and possibly on targeting brain-protective interventions earlier in those with evidence of silent cardiovascular damage.
Elevated levels of cardiac injury biomarkers (especially high-sensitivity troponin) measured in mid-life are associated with an increased risk of dementia many years later, potentially reflecting that silent heart damage is setting the stage for brain aging/neurovascular injury. While this doesn’t prove causation, it strengthens the notion that the heart-brain connection is significant and that protecting cardiovascular health may help reduce dementia risk. If you like, I can pull up the full study details (sample size, follow-up years, exact biomarker levels, cognitive outcomes) and we can discuss how strong the evidence is and what it might mean for clinical practice. Would you like that?
Additionally, scientists discovered that study participants with high levels of troponin between the ages of 45 and 69 experienced a quicker decline in their memory, thinking, and problem-solving abilities. These participants also tended to have a smaller hippocampus and lower gray matterTrusted Source brain volume, both of which are signs of dementia. Poor heart health in middle age puts people at increased risk of dementia in later life,
Damage to the brain seen in people with dementia accumulates slowly over the decades before symptoms develop. Control of risk factors common to both heart disease, stroke, and dementia in middle age, such as high blood pressure, may slow or even stop the development of dementia as well as cardiovascular disease. We now need to carry out studies to investigate how well troponin levels in the blood can predict future dementia risk. Our early results suggest that troponin could become an important component of a risk score to predict the future probability of dementia.