The BALTAZAR Study: How Caffeine Intake Affects Alzheimer's Biomarkers

Caffeine, one of the most commonly consumed psychoactive substances, has been linked to potential neuroprotective benefits in several large-scale studies. However, few studies have directly examined how caffeine consumption relates to key Alzheimer's disease (AD) biomarkers in people with cognitive impairments.

The Study

The BALTAZAR study, titled "Association of Caffeine Consumption with Cerebrospinal Fluid Biomarkers in Mild Cognitive Impairment and Alzheimer’s Disease," investigates whether regular caffeine intake affects Alzheimer's disease biomarkers in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) and AD. The study focuses on two key biomarkers, amyloid beta and tau proteins, which play central roles in the development of AD. The research builds on previous evidence suggesting caffeine could help protect against cognitive decline and neurodegenerative diseases like Alzheimer’s.

Study Design & Methods

The study included 263 participants: 147 with MCI (40 non-amnestic and 107 amnestic) and 116 with Alzheimer's disease. All were part of the Biomarker of AmyLoid pepTide and AlZheimer’s diseAse Risk (BALTAZAR) cohort, recruited from 23 memory centers across France between 2010 and 2015.

Caffeine consumption was assessed through a self-reported survey completed by the patients and their caregivers. This survey recorded daily caffeine intake from sources like coffee, tea, chocolate, and sodas. Participants were then divided into two groups: low caffeine intake (≤216 mg/day) and high caffeine intake (>216 mg/day).

The researchers used statistical models to analyze the relationship between caffeine consumption and CSF biomarker levels, adjusting for factors like age, gender, APOE ε4 carrier status, education level, and smoking habits.

Key Findings

The study found that lower caffeine intake was linked to worse cognitive outcomes. Patients who consumed less caffeine were more likely to be classified as having amnestic MCI or Alzheimer’s disease compared to those who consumed more caffeine. This relationship held even after accounting for confounding factors like age, smoking, and APOE ε4 status.

Lower caffeine intake was also associated with lower levels of the Aβ1-42 protein and a reduced Aβ1-42/Aβ1-40 ratio—both markers of increased amyloid buildup in the brain, a key feature of Alzheimer's progression. This suggests that higher caffeine intake might help protect against amyloid accumulation. However, no significant relationship was found between caffeine consumption and CSF tau or p-tau levels, leaving caffeine’s impact on tau pathology unclear.

Conclusion

The BALTAZAR study provides evidence that higher caffeine intake may have beneficial effects on memory and Alzheimer's biomarkers in individuals with MCI and AD. The findings support previous studies that suggest caffeine could protect against cognitive decline, particularly by influencing amyloid-related processes. However, its effect on tau pathology remains uncertain.

The researchers emphasize the need for further research, including clinical trials, to explore caffeine’s long-term impact on cognitive function and AD biomarkers—particularly its influence on tau.

Reference

Blum, D., Cailliau, E., Hélène Béhal, Vidal, J., Delaby, C., Luc Buée, Allinquant, B., Gabelle, A., Stéphanie Bombois, Lehmann, S., Schraen‐Maschke, S., & Hanon, O. (2024). Association of caffeine consumption with cerebrospinal fluid biomarkers in mild cognitive impairment and Alzheimer’s disease: A BALTAZAR cohort study. Alzheimer S & Dementia. https://doi.org/10.1002/alz.14169