Caffeine and Alzheimer’s disease: Moderate intake may slow cognitive decline

A new scientific review published in Cureus suggests that moderate caffeine consumption might help protect against the progression of Alzheimer’s disease, especially in individuals with mild cognitive impairment. Although the evidence is not entirely consistent, the findings point toward a possible dose-dependent relationship, with higher caffeine levels associated with slower cognitive decline.

Alzheimer’s disease is the most common form of dementia, affecting millions of people worldwide. As life expectancy increases, the number of individuals living with Alzheimer’s is expected to rise significantly, tripling by 2050. This has sparked a global effort to identify factors that could slow or prevent the disease’s progression. Since current treatments offer only limited relief, researchers are increasingly exploring lifestyle factors—such as diet, exercise, and sleep—for their potential protective effects. Caffeine, found in coffee, tea, and other beverages, is one such factor under investigation.

Caffeine is one of the most widely consumed substances in the world. It stimulates the brain, increases alertness, and improves mood. But scientists have also been exploring whether its effects go deeper—perhaps even helping to protect the brain against neurodegenerative diseases like Alzheimer’s. Animal studies have shown that caffeine can reduce the buildup of harmful proteins in the brain. Human research has produced mixed results, but some studies have reported that regular coffee drinkers tend to have lower rates of cognitive decline.

To better understand the potential link between caffeine intake and Alzheimer’s progression, a team of researchers from institutions in Pakistan, the United Kingdom, and the United States conducted a systematic review. They examined studies from major scientific databases to identify those that looked at how caffeine consumption affected the risk of developing Alzheimer’s or the progression from mild cognitive impairment to full-blown dementia.

The review included four studies that met strict inclusion criteria. One of the most compelling pieces of evidence came from a study that measured caffeine levels in the blood of people with mild cognitive impairment. Those with higher plasma caffeine levels—above 1200 nanograms per milliliter—did not go on to develop dementia during the study period. In contrast, those with lower levels had a significantly higher risk of progressing to Alzheimer’s.

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Another study from the BALTAZAR cohort, a large European sample, found that individuals who consumed less than 216 milligrams of caffeine per day—roughly two cups of coffee—had more memory problems and worse biological markers associated with Alzheimer’s. This supports the idea that a threshold amount of caffeine may be needed to see protective effects.

A genetic study using data from the UK Biobank added more nuance to the picture. Researchers used a method called Mendelian randomization, which looks at genetic variants associated with naturally higher caffeine levels in the blood. They found a modest protective effect, but the result did not reach statistical significance. Still, it suggested that the connection between caffeine and brain health could be partly influenced by how each person’s body processes caffeine.

Another long-term study from Portugal compared people with Alzheimer’s to healthy individuals. Over the 20 years leading up to diagnosis, those who developed Alzheimer’s had consumed less caffeine than those who remained cognitively healthy. After accounting for other health conditions, this pattern remained.

Overall, the review suggests that moderate caffeine intake—generally over 200 milligrams per day—may offer some protection against Alzheimer’s disease. This protective effect seems to be strongest in people with mild cognitive impairment, a condition that often precedes Alzheimer’s but doesn’t yet cause major disruptions in daily life. Caffeine may help delay or prevent the transition from this early stage to full dementia.

The researchers also examined potential biological explanations for the effect. Caffeine blocks adenosine receptors in the brain, which can reduce inflammation and support better communication between brain cells. It may also help limit the accumulation of amyloid-beta, a protein that forms plaques in the brains of people with Alzheimer’s. Other studies have shown that caffeine boosts levels of brain-derived neurotrophic factor, a molecule that supports learning and memory by strengthening connections between neurons.

The review highlights several factors that may influence the relationship between caffeine and Alzheimer’s. Genetics play a role, especially in how the body breaks down caffeine. For example, people with certain versions of the CYP1A2 gene metabolize caffeine more slowly, which could affect how long it stays active in the body. Timing also matters. People who have consumed caffeine regularly over many years, particularly during midlife, seem to benefit more than those who start later in life.

Although these findings are encouraging, the researchers caution that the evidence is still incomplete. The four studies included in the review varied widely in design, participant populations, and methods of measuring caffeine intake. Some relied on self-reported dietary surveys, while others used blood tests. These differences make it hard to draw firm conclusions or recommend specific intake levels for everyone.

Another limitation is that most of the studies were observational. They can show associations, but they can’t prove that caffeine directly causes a reduction in Alzheimer’s risk. It’s possible that people who drink more coffee also engage in other healthy behaviors that contribute to better brain health, such as regular physical activity or a healthy diet.

The researchers call for more well-designed clinical trials that can test how different amounts of caffeine affect brain health over time. They also suggest studying different sources of caffeine—like coffee, tea, or chocolate—to determine whether the benefits come from caffeine itself or from other compounds found in these foods and drinks.

The study, “Association Between Caffeine Intake and Alzheimer’s Disease Progression: A Systematic Review,” was authored by Zarbakhta Ashfaq, Zainab Younas, Eemaz Nathaniel, Abdur Rehman, Arzoo Siddiqi, Naveed Rasool, and Maaz Amir.