A study of individuals with mild cognitive impairment and Alzheimer’s disease in France found that participants who consumed less caffeine had 2.49 times higher odds of having amnestic mild cognitive impairment and worse levels of specific cerebrospinal fluid biomarkers associated with Alzheimer’s. The study was part of the ongoing BALTAZAR cohort and was published in the journal Alzheimer’s & Dementia.
Alzheimer’s disease is a progressive neurodegenerative disorder that profoundly affects memory, thinking, and behavior. It is the most common cause of dementia, particularly in older adults, though in rare cases, it can develop in younger people. Alzheimer’s disease is characterized by the buildup of abnormal clumps of protein fragments called amyloid-beta plaques and twisted fibers of tau protein, known as tau tangles, in the brain. These proteins disrupt the communication between brain cells and eventually lead to their death, causing cognitive decline and memory loss.
Early symptoms of Alzheimer’s often include difficulty remembering recent events or conversations. As the disease progresses, more severe symptoms emerge, including disorientation, confusion, difficulty speaking or writing, and changes in personality or mood. In advanced stages, individuals lose the ability to carry out everyday tasks, such as cooking or dressing, and require full-time care. Currently, there is no cure for Alzheimer’s, though there are treatments aimed at temporarily alleviating symptoms.
Study author David Blum and his colleagues wanted to explore the relationship between habitual caffeine intake and certain biomarkers related to Alzheimer’s disease in the cerebrospinal fluid—the fluid that surrounds the brain and spinal cord. These biomarkers include amyloid-beta and tau proteins, which are used to detect and monitor the progression of Alzheimer’s disease. The team also examined the differences in caffeine consumption between individuals with mild cognitive impairment, a condition that often precedes Alzheimer’s, and those who had already been diagnosed with Alzheimer’s disease.
The study was part of the BALTAZAR cohort, a large, ongoing research project focusing on individuals with mild cognitive impairment and Alzheimer’s disease. The researchers analyzed 263 participants: 147 with mild cognitive impairment and 116 with Alzheimer’s disease. Mild cognitive impairment (MCI) participants were further categorized into two subtypes: amnestic mild cognitive impairment (aMCI), where memory loss is the primary issue, and non-amnestic mild cognitive impairment (naMCI), where other cognitive functions are primarily affected.
Participants in the study completed a detailed survey about their daily consumption of caffeine-containing items, such as coffee, tea, chocolate, or sodas. This survey was designed to assess each participant’s caffeine intake, which was calculated in milligrams per day. Alongside the caffeine survey, participants also provided blood samples and cerebrospinal fluid samples.
Cerebrospinal fluid was analyzed for key biomarkers of Alzheimer’s disease, including total tau (tau), phosphorylated tau (p-tau181), amyloid-beta 1-42 (Aβ1-42), and amyloid-beta 1-40 (Aβ1-40). Elevated levels of tau and p-tau181 indicate brain cell damage and neurofibrillary tangles, which are associated with Alzheimer’s disease. On the other hand, lower levels of Aβ42, particularly in relation to Aβ40, are associated with the buildup of amyloid plaques, another indicator of Alzheimer’s disease progression.
Participants were categorized into two groups based on their caffeine consumption: a “low caffeine” group, with daily intake below 216 milligrams, and a “high caffeine” group, with daily intake above this amount. The researchers then compared the cognitive status and biomarker levels between these two groups.
Results showed that individuals who consumed lower amounts of caffeine had significantly higher odds of being categorized as amnestic, meaning they experienced memory-related impairments. Specifically, the odds of being diagnosed with amnestic mild cognitive impairment or Alzheimer’s disease were 2.49 times higher for participants with lower caffeine consumption compared to those with higher intake. This suggests a potential protective effect of caffeine on memory, particularly in individuals at risk for or already diagnosed with Alzheimer’s disease.
When the researchers looked specifically at participants with mild cognitive impairment, they found that those with lower caffeine intake had 2.72 times higher odds of being classified as amnestic rather than non-amnestic. This finding suggests that caffeine consumption might be particularly relevant for memory-related issues.
In addition to cognitive outcomes, the study also found significant differences in cerebrospinal fluid biomarkers between high and low caffeine consumers. Participants who consumed less caffeine tended to have lower levels of Aβ42 and lower Aβ42/Aβ40 and Aβ42/p-tau181 ratios. These lower levels and ratios of Aβ42 are typically associated with increased amyloid plaque formation in the brain, a major hallmark of Alzheimer’s disease. The results suggest that lower caffeine intake might be linked to greater amyloid burden, which is associated with faster disease progression.
“Our data support an association of lower caffeine consumption with a higher risk of being amnestic as well as with deleterious changes in CSF [cerebrospinal fluid] biomarkers of MCI [mild cognitive impairment] and AD [Alzheimer’s disease] patients,” the study authors concluded.
The study sheds light on the association between caffeine consumption and the symptoms of Alzheimer’s disease. However, it should be noted that the design of this study does not allow for any cause-and-effect conclusions to be drawn from the data. While it is possible that caffeine might have protective effects against the symptoms of Alzheimer’s, it is also possible that individuals in better cognitive health simply consume more caffeinated beverages (e.g., because they are better able to take care of themselves, including being better able to obtain and prepare the beverages they prefer).
The paper, “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.
