Coffee or Tea? Caffeine Consumption— a New Perspective of Dementia Prevention

Dementia is a growing global health concern, with rising prevalence driven by population ageing and limited curative treatment options. Consequently, preventive strategies have become a central focus of research. Among modifiable lifestyle factors, caffeine consumption—particularly through widely consumed beverages such as coffee and tea—has attracted increasing attention for its potential neuroprotective effects. This article reviews current evidence on the association between caffeinated coffee and tea intake and the risk of dementia, highlighting epidemiological findings that suggest a non-linear, dose-dependent relationship, in which moderate consumption is linked to the greatest risk reduction. Proposed biological mechanisms include adenosine receptor antagonism, inhibition of amyloid precursor protein processing, and antioxidant and anti-inflammatory effects. Differences between coffee and tea are also explored, with tea containing additional bioactive compounds such as epigallocatechin gallate and L-theanine that may enhance cognitive benefits. Despite promising findings, the underlying mechanisms remain incompletely understood, and direct comparisons between coffee and tea are limited. Overall, these findings underscore the importance of moderate caffeine intake within a broader framework of lifestyle-based dementia prevention.

Introduction

Dementia is a chronic syndrome that causes cognitive decline in affected patients, usually in the elderly.1,2 It is estimated that dementia affects up to 57 million people worldwide and is projected to reach 152.8 million cases by 2050, because of population ageing, making it a prominent global public health concern.3,4 The treatments currently available mainly focus on management of symptoms, and are unable to cure the underlying diseases.5,6 Indeed, prevention remains the utmost focus of dementia research.7 While certain risk factors such as genetics and age cannot be changed, lifestyle choices—including blood pressure management, regular physical activity, smoking cessation, moderate alcohol consumption, and a healthy diet—can be modified to help preserve cognitive function.3,8 It is well known that common caffeinated beverages such as coffee and tea possess potential cognitive benefits, especially in sleep-deprived individuals.9 Recent studies have even pointed out that moderate caffeine consumption may be associated with lower risk of dementia.10,11

What are Dementia and Cognitive Decline?

As aforementioned, dementia is an umbrella term for a syndrome—not a specific disease—characterised by a chronic, progressive decline in cognitive function severe enough to interfere with daily life. It is caused by various underlying neurodegenerative conditions and brain injuries, with over 100 identified types and causes.2,3 The most common types of dementia include Alzheimer’s disease (AD), vascular dementia, and Lewy body dementia.12 Rarer dementia types also include frontotemporal dementia, young-onset dementia, or when multiple dementia types are present, mixed dementia.13

Dementia symptoms present differently across patients and are shaped by the stage and progression of the disease. Early-stage dementia (Stages 1–3) is typically characterized by memory impairment and deficits in reasoning, communication, planning, and organizational skills.2,3,14 In middle-stage dementia (Stages 4–5), the patient’s mood, behaviour, and even personality (more common in the case of frontotemporal dementia) may change, leading to struggle with daily tasks and loss of independence.2,3,14,15 In the final stage of dementia (Stages 6–7), patients may experience severe cognitive decline, and exacerbation of the aforementioned symptoms.14 Ultimately, dementia alters nearly every aspect of daily living, profoundly impacting both patients and their caregivers.

In addition to its many debilitating symptoms, dementia also induce emotional distress in patients. Emotional distress in dementia is often a signal of an unmet need or physical discomfort, rather than just a symptom of the disease. It can manifest as agitation, crying, wandering, or aggression.16 Insecurity, anxiety, and social stigma collectively exacerbate the psychological decline experienced by individuals with dementia.15,17

Such distress can extend to caregivers, manifesting in deteriorating physical health and psychological resilience.18,19 It is important to note that dementia also imposes a significant burden on healthcare systems. According to an estimate, direct health care spending attributable to Alzheimer's disease and related dementias (ADRD) will reach $1.6 trillion in 2050, or 9.4% of projected health spending worldwide.20,21

Early intervention and prevention of dementia are thought to be beneficial. Barnett et al. demonstrated in their symptomatic treatment model that a maximum net benefit would be produced 8 years prior to a standard diagnosis, with efficacy decreasing by 17% for every year that interventions were delayed.22 The results were even more pronounced in their disease-modifying model, the maximum net benefit being 15 times larger than that of the symptomatic treatment.22 Their findings are consistent with previous research, indicating the necessity of early interventions by means of cognitive training, and lifestyle changes such as physical activity, psychosocial support, and dieting.23,24

Association between Caffeine and Dementia

Research has shown that caffeine consumption is associated with a lower risk of dementia. Zhang et al. performed a prospective cohort study on participants without cancer, Parkinson disease, or dementia at the time of entry to elucidate the association between caffeine consumption, cognitive functioning, and dementia.11 After adjusting for potential confounders, there were 330 cases per 100,000 persons-years in the lowest consumption quartile of caffeinated coffee, while there were 141 cases per 100,000 persons-years in the highest consumption quartile, resulting in a hazard ratio of 0.82 (95% CI, 0.76-0.89).11 A similar effect is observed in tea consumption: 321 per 100,000 person-years for the tertile of lowest tea intake and 201 per 100,000 person-years for the tertile of highest tea intake.11 Both results, supported by other reviews and analyses, suggest a protective effect of caffeine against dementia.10,11,25,26

Across multiple studies, the relationship between caffeine consumption and dementia is considered non-linear. Zhang et al. demonstrated through dose-response analyses that caffeine consumption was inversely associated with dementia risk in a non-linear manner (Figure 1).11 This finding is consistent with other meta-analyses and reviews, commonly suggesting a J-shaped or U-shaped dose-response graph.10,25,26 Thus, it is suggested that moderate consumption of caffeinated coffee has the most effective neuroprotective effect against dementia.10,11, 25,26 This observation prompts important questions regarding the biological mechanisms that may drive such a unique dose–response relationship.

Figure 1: Association between Dementia and Caffeinated Coffee Intake.11 c/d: cups per day; CI: confidence interval

Proposed Mechanism of Action for Neuroprotection

A prominent mechanism proposed is the antagonistic nature of caffeine against adenosine receptors. The blocking of both A1 and A2A receptors have been shown to impede the pathological changes induced by amyloid β25-35 (Aβ25-35), a highly toxic, 11-amino-acid fragment of the full-length Aβ protein.7 Thus, caffeine may exert its neuroprotective effects via decreasing protein misfolding and Aβ plaque formation.27

Another hypothesised mechanism for caffeine’s neuroprotective property is its inhibition of amyloid precursor protein (APP) processing. Caffeine is said to suppress β- and γ-secretase activity.11 β-secretase is responsible for the proteolytic cleavage and subsequent generation of membrane-tethered C-terminal fragments (CTF) from APP.7 Caffeine stimulates protein kinase A (PKA) activity and reduces nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), resulting in the inactivation of β-secretase.28 CTFs are often directly subjected to a second cleavage by the γ-secretase complex, producing multiple Aβ isoforms, namely the highly neurotoxic Aβ1-42.7 Caffeine reduces glycogen synthase kinase-3 alpha (GSK-3α) levels, thereby diminishing γ-secretase activity.28

Antioxidant and anti-neuroinflammatory properties of caffeine may also contribute to its neuroprotective effects. Neuronal oxidative stress is a primary driver of neuronal damage in both AD and vascular dementia.29 Caffeine can act as an antioxidant by inactivating NF-κB and decreasing reactive oxygen species generation.7,30 By directly suppressing the nuclear translocation of NF-κB and its subsequent transcriptional events, caffeine also helps reduce neuroinflammation.7 Decreased NF-κB production reduces downstream production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumour necrosis factor-alpha (TNF-α), protecting oligodendrocytes and astrocytes from inflammatory damage.31

The elevated risk of dementia associated with high caffeine intake is likely multifactorial. Recall the non-linearity of the dose-response curve of caffeine against dementia risk—evidence suggests that the neuroprotective effects of caffeine may diminish at higher levels of consumption.11 A plausible explanation includes a physiological threshold for caffeine absorption, disruption of sleep quality, and exacerbation of anxiety.11 These adverse effects may counteract the potential cognitive benefits of caffeine.

Differences between Caffeinated Coffee and Tea in Neuroprotection

Despite the lack of randomised clinical trials comparing the neuroprotective properties of caffeinated coffee and tea, much research has shown consistent association between tea consumption and cognitive function.32 The presence of epigallocatechin-3-gallate (EGCG) and L-theanine in tea may increase the neuroprotective capacity of tea consumption.11 EGCG has been proven to improve cognitive functioning in cognitive-deficit diseases such as AD, albeit without a clear explanation of its mechanism of action.33 Similarly, L-theanine improves cognitive functions—better performance is observed in the L-theanine group than control in terms of attention and working memory tasks.34 Therefore, it would seem that the bioactive compounds present in tea may promote more consistent improvements in cognitive function compared to those associated with caffeinated coffee consumption.

On the other hand, caffeinated coffee consumption may be likely to have more pronounced effect in neuroprotection. Zhang et al. computed the hazard ratios of each tertile/quartile of caffeinated coffee and tea consumption against the lowest consumption group (the first tertile/quartile). It appeared that except for the second lowest intake tertile/quartile, the caffeinated coffee group showed lower hazard ratios (Figure 2).11

However, due to the lack of head-to-head studies comparing the neuroprotective effects of caffeinated coffee and tea, there is no conclusive answer as to which offers greater benefits,

Figure 2: Neuroprotective Effects of Caffeinated Coffee and Tea.11

So… Coffee or Tea?

Although current evidence suggests that caffeinated coffee and tea may be associated with a reduced risk of dementia, the underlying mechanisms remain incompletely understood and require further investigation. For individuals concerned about dementia prevention, it is important to recognise that any potential neuroprotective benefit appears to be linked to moderate consumption rather than excessive intake. Ultimately, the question should perhaps not be framed as simply “coffee or tea”, but rather considered within the context of a broader lifestyle approach—one that includes a balanced diet, regular physical activity, cognitive engagement, adequate sleep, good mental well-being, avoidance of excessive alcohol consumption, and consultation with a healthcare professional when appropriate.22,23

Conclusion

Current evidence suggests that caffeinated coffee and tea may contribute to a reduced risk of dementia, particularly when consumed in moderation. However, the relationship is complex and appears to follow a non-linear pattern, with excessive intake potentially diminishing the benefits. While several plausible biological mechanisms have been proposed, including modulation of amyloid pathways and neuroinflammation, definitive causal pathways remain to be fully established. Furthermore, although both coffee and tea demonstrate potential neuroprotective properties, insufficient comparative evidence prevents a clear conclusion regarding their relative effectiveness.

Importantly, caffeine consumption should not be viewed in isolation. The prevention of dementia is best approached through a comprehensive lifestyle strategy that integrates a balanced diet, regular physical activity, cognitive engagement, adequate sleep, and good mental health, alongside avoidance of excessive alcohol intake and appropriate medical consultation. Future research, particularly well-designed clinical and mechanistic studies, is needed to clarify the role of caffeine and its interaction with other lifestyle factors in dementia prevention.

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