Early cognitive ability and dementia risk: Patterns beyond education and mortality

1.

The national cohort study by Kremen et al. presents compelling evidence that general cognitive ability (GCA), measured in young adulthood, is a stronger predictor of the risk of dementia than education attainment. ¹ Although this study exhibits promising results, its data reveal several under‐recognized patterns that merit further consideration and discussion.

A notable observation is that GCA's protective effect against dementia becomes more pronounced when early mortality is taken into account. The hazard ratio (HR) for GCA improves from 0.865 to 0.836 after adjustment, ¹ suggesting that individuals with lower GCA may die before their dementia risk fully manifests. This stronger association implies that GCA contributes not only to delayed cognitive decline but also to overall survival. Indeed, the mortality HR for GCA was 0.821, ¹ reinforcing the view that cognitive ability supports broader resilience—potentially through better decision making, executive function, and health literacy. ² , ³ In contrast, although education lost significance as an independent predictor of dementia when GCA was included, it remained significantly associated with lower mortality (HR = 0.912), ¹ indicating indirect health benefits through behavioral, social, or economic pathways. ⁴

Another underappreciated result is the statistically significant association between physical activity and reduced dementia risk, which became evident only in mortality‐adjusted models (HR = 0.884; P = 0.039). ¹ This suggests that physically inactive individuals may have been lost to follow‐up through premature death, obscuring the protective role of physical activity in unadjusted analyses. That this association persists after adjusting for GCA and socioeconomic status affirms its relevance as a modifiable, independent protective factor. It also underscores the value of behavioral interventions even in populations with high early‐life cognitive ability. ⁵ Although the authors did not model interaction terms, their reported HRs for low GCA (1.164) and low education (1.288) imply a compounded vulnerability for individuals low in both. A simple multiplicative model yields a crude estimated joint HR of ≈ 1.5, indicating a nearly 50% increased risk of dementia for this subgroup. This intersectional risk highlights the need for preventive strategies that focus not only on single variables but on the accumulation of disadvantage in cognitive and educational dimensions.

Equally striking is the observed cohort gradient in dementia cases. More than half of all dementia diagnoses originated from men born between 1954 and 1958, while only 7.2% occurred in those born after 1969, despite comparable follow‐up durations. ¹ This pattern likely reflects real generational improvements in early life nutrition, health‐care access, and education quality. ⁴ , ⁶ It reinforces the idea that macro‐level developmental investments can reduce cognitive morbidity decades later—empirically supporting policy efforts that target early childhood environments.

Several limitations in the study constrain the interpretation and generalizability of its findings. Most prominently, the all‐male, Swedish sample precludes insights into sex‐specific pathways of cognitive aging. Prior research has shown that women exhibit distinct cognitive reserve mechanisms, including advantages of verbal fluency and hormonally influenced resilience. ⁷ , ⁸ Thus, extrapolation to female populations should be made cautiously. Additionally, the use of military conscription records introduces selection bias by excluding individuals with pre‐existing cognitive or psychiatric impairments, potentially underestimating the variability in GCA and its association with later outcomes.

Another conceptual issue concerns the timing of the GCA measurement. Assessing cognitive ability at 18 years of age, after substantial education exposure, risks treating it as fully antecedent. In reality, GCA and education are likely to influence each other, shaped by early life adversity and socioeconomic background. ² , ⁹ Without developmental data from childhood, causal inference remains uncertain.

Finally, dementia diagnoses were derived from registry‐based International Classification of Diseases codes, with limited clinical or biomarker validation. This raises concerns about misclassification between dementia subtypes, such as Alzheimer's disease and vascular dementia, each of which may interact differently with reserve factors like GCA and education. ¹⁰

In summary, we commend the work of Kremen et al. to establish GCA as a key predictor of dementia. ¹ However, this discussion draws attention to its amplified effect after mortality adjustment, the obscured role of physical activity, and the compounded risk from low GCA and education levels. These observations reinforce the case for preventive efforts throughout the lifespan.

AUTHOR CONTRIBUTIONS

Chung‐Hsin Yeh: conceptualization, methodology, investigation, formal analysis, validation, writing‐original draft, and writing‐review and editing. Shiuan‐Chih Chen: conceptualization, methodology, investigation, formal analysis, supervision, validation, and writing—review and editing.

CONFLICT OF INTEREST STATEMENT

The authors have no conflicting interests to declare. Any author disclosures are available in the supporting information.

Supporting information

Supporting Information