United States: A French investigation into individuals grappling with mild cognitive impairment (MCI) and Alzheimer’s disease revealed a compelling correlation: participants with diminished caffeine consumption exhibited a 2.49-fold heightened likelihood of amnestic MCI alongside unfavorable cerebrospinal fluid biomarkers linked to Alzheimer’s pathology. The research, stemming from the ongoing BALTAZAR cohort, was unveiled in the journal Alzheimer’s & Dementia.
Alzheimer’s disease, a relentless neurodegenerative disorder, devastates memory, cognition, and behavior. As the leading cause of dementia, predominantly in aging populations, its impact can be particularly severe, though rarer cases emerge in younger individuals. This disease is typified by the accumulation of abnormal protein fragments, notably amyloid-beta plaques and tau tangles, within the brain. These proteins interfere with neuron-to-neuron communication, ultimately leading to neuronal death, driving cognitive deterioration and memory erosion.
Initial symptoms of Alzheimer’s often include challenges in recollecting recent events or dialogues. As the affliction advances, symptoms escalate—disorientation, difficulty in articulating thoughts or writing, and drastic personality shifts become prevalent. In later stages, sufferers lose the capacity to perform daily tasks like cooking or dressing, necessitating constant care. Currently, no cure exists, although some treatments aim to temporarily ease symptoms.
David Blum, the study’s primary author, and his collaborators delved into the interplay between regular caffeine intake and Alzheimer’s biomarkers present in cerebrospinal fluid, a key indicator surrounding the brain and spinal cord. They specifically focused on amyloid-beta and tau proteins, utilized to monitor Alzheimer’s progression. The team also explored the disparity in caffeine consumption among individuals with MCI, often a precursor to Alzheimer’s, and those already diagnosed with the disease.
This study, nested within the broader BALTAZAR cohort, analyzed 263 participants: 147 with MCI and 116 with Alzheimer’s. MCI participants were further classified into two types: amnestic MCI (aMCI), where memory impairments predominate, and non-amnestic MCI (naMCI), where other cognitive faculties are primarily affected.
Through an exhaustive survey, participants detailed their daily intake of caffeine from sources like coffee, tea, chocolate, or sodas. This survey quantified each individual’s caffeine consumption in milligrams per day. Blood and cerebrospinal fluid samples were collected alongside the survey.
Cerebrospinal fluid underwent analysis to detect critical Alzheimer’s biomarkers, including total tau (tau), phosphorylated tau (p-tau181), amyloid-beta 1-42 (Aβ1-42), and amyloid-beta 1-40 (Aβ1-40). Elevated tau and p-tau181 levels signify brain cell damage and the presence of neurofibrillary tangles, integral to Alzheimer’s progression. Conversely, reduced Aβ42 levels, particularly in relation to Aβ40, indicate amyloid plaque accumulation, another hallmark of Alzheimer’s advancement.
Participants were divided into two groups based on their caffeine consumption: the “low caffeine” group (intake below 216 milligrams daily) and the “high caffeine” group (intake above this threshold). Researchers compared cognitive status and biomarker levels between these two groups.
The findings revealed that participants with lower caffeine consumption faced significantly greater odds of being classified as amnestic. Specifically, the risk of being diagnosed with aMCI or Alzheimer’s was 2.49 times higher for those with lower caffeine intake, suggesting that caffeine may exert a protective influence on memory, particularly for those vulnerable to or diagnosed with Alzheimer’s.
Focusing on the MCI participants, researchers noted that those with lower caffeine intake had a 2.72-fold increased likelihood of being classified as amnestic versus non-amnestic. This suggests that caffeine consumption could hold particular relevance in relation to memory-related difficulties.
Beyond cognitive outcomes, the study also highlighted substantial differences in cerebrospinal fluid biomarkers between low and high-caffeine consumers. Those consuming less caffeine exhibited reduced Aβ42 levels and lower Aβ42/Aβ40 and Aβ42/p-tau181 ratios. These lower values typically correspond to increased amyloid plaque formation in the brain, a significant indicator of Alzheimer’s disease progression. This suggests that reduced caffeine intake may be linked to a greater amyloid burden, which correlates with the disease’s faster advancement.
“Our data reinforces the association between lower caffeine consumption and a higher likelihood of amnestic classification, as well as deleterious shifts in cerebrospinal fluid biomarkers among patients with MCI and Alzheimer’s,” the authors concluded.
Although this study illuminates a potential link between caffeine intake and Alzheimer’s symptoms, its design does not permit the drawing of cause-and-effect conclusions. While caffeine may possess protective properties against Alzheimer’s, it is equally plausible that individuals with better cognitive function tend to consume more caffeinated beverages due to their greater ability to procure and prepare these drinks.
The paper, entitled Association of Caffeine Consumption with Cerebrospinal Fluid Biomarkers in Mild Cognitive Impairment and Alzheimer’s Disease: A BALTAZAR Cohort Study, was authored by David Blum, Emeline Cailliau, Hélène Béhal, Jean-Sébastien Vidal, Constance Delaby, Luc Buée, Bernadette Allinquant, Audrey Gabelle, Stéphanie Bombois, Sylvain Lehmann, Susanna Schraen-Maschke, and Olivier Hanon.