Considerable controversy exists about the role of education in the risk of dementia. Individual studies have not been conclusive so far. To examine the hypothesis that lower education is associated with a higher risk of dementia, we carried out a meta-analysis. Observational studies published as of October 2005 that examined the association between education and risk of dementia were systematically reviewed. Relative risks (RRs) and odds ratios were extracted from cohort and case-control studies. We first compared the risk of dementia in subjects with high level of education with the risk of dementia in those with low educational level. In a subsequent analysis, we compared the risk of persons with high education with the risk of subjects with education level other than high (medium, low). We weighted log RRs for cohort studies or odds ratios by the inverse of their variances. Nineteen studies were included in our meta-analysis (13 cohort and 6 case-control studies). RRs for low versus high education level were: Alzheimer’s disease (AD) 1.80 (95% CI: 1.43–2.27); non-AD dementias, 1.32 (95% CI: 0.92–1.88), and all dementias 1.59 (95% CI: 1.26–2.01). For low and medium versus high education level, the RRs were: AD 1.44 (95% CI: 1.24–1.67); non-AD 1.23 (95% CI: 0.94–1.61), and all dementias 1.33 (95% CI: 1.15–1.54). These results confirm that low education may be a risk factor for dementia, especially for AD.

Aims: Adolescence is usually the time when individuals first drink alcohol and this has been associated with relatively weak or immature inhibitory control. This review examines the changes on brain development and inhibitory function that take place during adolescence and youth as well as the relationship between inhibitory control and alcohol use at this early age. Methods: Narrative review of the chief studies related to (a) the development of inhibitory control during adolescence, (b) the deficits in the inhibitory ability in alcohol use disorders and (c) the effects of acute alcohol intake and binge drinking on inhibitory control in adolescents and young adults. Results: Inhibitory control processes are developing during adolescence and youth. Poor inhibitory functions may predispose the individual to alcohol misuse. Likewise, acute and binge alcohol drinking may impair the inhibitory control and compromise the ability to prevent or stop behaviour related to alcohol use. Conclusion: Poor inhibitory control can be both the cause and the consequence of excessive alcohol use. Adolescence and young adulthood may be a particularly vulnerable period due to (a) the weak or immature inhibitory functioning typical of this stage may contribute to the inability of the individual to control alcohol use and (b) alcohol consumption per se may alter or interrupt the proper development of inhibitory control leading to a reduced ability to regulate alcohol intake. Further longitudinal research is needed to evaluate the interaction between inhibitory control dysfunction and alcohol use in both situations.