TOPLINE:

Elevated cardiac troponin I levels during midlife — indicative of subclinical myocardial injury — were associated with a higher risk for dementia, faster cognitive decline, and greater brain atrophy in later life, with differences apparent up to 25 years before diagnosis.

METHODOLOGY:

• Researchers conducted a prospective study to evaluate whether subclinical myocardial injury during midlife, indexed by rising cardiac troponin I levels, predicts accelerated cognitive decline, smaller structural brain volume, and a higher risk for dementia.
• A total of 5985 British civil service participants (aged 45-69 years at baseline) recruited from the Whitehall II study were followed up for a median of 24.8 years through March 2023.
• All participants were free of dementia and cardiovascular disease and had cardiac troponin I levels measured at baseline.
• Cognitive function was assessed through a comprehensive test battery administered at six waves of clinical examination between 1997 and 2022, evaluating memory, executive function, and fluency domains.

TAKEAWAY:

• Each doubling of cardiac troponin I levels at baseline was associated with a 10% higher risk for dementia (hazard ratio, 1.10; 95% CI, 1.03-1.17), and levels above 5.2 ng/L conferred a 38% higher risk than levels below 2.5 ng/L.
• Participants with cardiac troponin I levels above 5.2 ng/L had a 0.10 SD lower global cognitive z score at the age of 80 years (95% CI, 0.02-0.18) and a 0.19 SD lower score at the age of 90 years (95% CI, 0.03-0.35) than those with levels below 2.5 ng/L, indicating approximately 1.4 and 2 years of accelerated cognitive ageing, respectively.
• Furthermore, participants with cardiac troponin I levels above 5.2 ng/L had 0.64% lower grey matter volume and an 18% higher risk for hippocampal atrophy than those with levels below 2.5 ng/L, corresponding to an age effect of 2.7 and 3 years, respectively.
• Cardiac troponin I levels were consistently higher in those who developed dementia than in control individuals, detectable between 7 and 25 years before diagnosis, indicating long-term elevation preceding clinical onset.

IN PRACTICE:

"Measurement of cardiac troponin I using a high-sensitivity assay in midlife may be useful in the early identification of a population at risk of cognitive decline and dementia," the authors wrote.

SOURCE:

This study was led by Yuntao Chen, Division of Psychiatry, University College London, London, England. It was published online on November 06, 2025, in European Heart Journal.

LIMITATIONS:

Despite the lengthy follow-up, the study might have underestimated differences in troponin trajectory between cases of dementia and control individuals due to attrition from illness or death. The inclusion of a predominantly White civil servant cohort may have limited generalisability, and the observational design precluded causal inference.

DISCLOSURES:

The Whitehall II study received support through grants from multiple organisations, including the Wellcome Trust, UK Medical Research Council, British Heart Foundation, and others. Some authors reported serving as unpaid trustees of a charitable organisation and as the chair of a university ethics committee and receiving honoraria and consulting fees from various diagnostic and pharmaceutical companies for participation in expert panels.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.