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Published January 1, 2015 | Version v1
Journal article Open

Does Caffeine Consumption Modify Cerebrospinal Fluid Amyloid-beta Levels in Patients with Alzheimer's Disease?

Creators

  • 1. Coimbra Univ Hosp, Dept Neurol, Coimbra, Portugal
  • 2. Aristotle Univ Thessaloniki, Mem & Dementia Ctr, GR-54006 Thessaloniki, Greece
  • 3. Copenhagen Univ Hosp, Dept Neurol, Danish Dementia Res Ctr, Copenhagen, Denmark
  • 4. Univ Athens, Fac Med, Dept Neurol, Athens 11528, Greece
  • 5. Univ Gothenburg, Sahlgrenska Univ Hosp, Sahlgrenska Acad, Inst Neurosci & Physiol, Molndal, Sweden
  • 6. Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal

Description

Caffeine may be protective against Alzheimer's disease (AD) by modulating amyloid-beta (A beta) metabolic pathways. The present work aimed to study a possible association of caffeine consumption with the cerebrospinal fluid (CSF) biomarkers, particularly A beta. The study included 88 patients with AD or mild cognitive impairment. The consumption of caffeine and theobromine was evaluated using a validated food questionnaire. Quantification of caffeine and main active metabolites was performed with liquid chromatography coupled to tandem mass spectrometry. The levels of A beta(1-42), total tau, and phosphorylated tau in the CSF were determined using sandwich ELISA methods and other A beta species, A beta(X-38), A beta(X-40), and A beta(X-42), with the MSD A beta Triplex assay. The concentration of caffeine was 0.79 +/- 1.15 mu g/mL in the CSF and 1.20 +/- 1.88 mu g/mL in the plasma. No correlation was found between caffeine consumption and A beta(42) in the CSF. However, a significant positive correlation was found between the concentrations of theobromine, both in the CSF and in the plasma, with A beta(42) in the CSF. Theobromine in the CSF was positively correlated with the levels of other xanthines in the CSF, but not in the plasma, suggesting that it may be formed by central metabolic pathways. In conclusion, caffeine consumption does not modify the levels of CSF biomarkers, and does not require to be controlled for when measuring CSF biomarkers in a clinical setting. Since theobromine is associated with a favorable A beta profile in the CSF, the possibility that it might have a protective role in AD should be further investigated.

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