The Satisfaction with Life Scale (SWLS) has been widely used and has proven to be a valid and reliable instrument for assessing satisfaction with life in diverse population groups, however, research on satisfaction with life and validation of different measuring instruments in Mexican adults is still lacking. The objective was to evaluate the psychometric properties of the Satisfaction with Life Scale (SWLS) in a representative sample of Mexican adults. This is a methodological study to evaluate a satisfaction with life scale in a sample of 13,220 Mexican adults 50 years of age or older from the 2012 Mexican Health and Aging Study. The scale’s reliability (internal consistency) was analysed using Cronbach’s alpha and inter-item correlations. An exploratory factor analysis was also performed. Known-groups validity was evaluated comparing good-health and bad-health participants. Comorbidity, perceived financial situation, self-reported general health, depression symptoms, and social support were included to evaluate the validity between these measures and the total score of the scale using Spearman’s correlations. The analysis of the scale’s reliability showed good internal consistency (α = 0.74). The exploratory factor analysis confirmed the existence of a unique factor structure that explained 54% of the variance. SWLS was related to depression, perceived health, financial situation, and social support, and these relations were all statistically significant (P < .01). There was significant difference in life satisfaction between the good- and bad-health groups. Results show good internal consistency and construct validity of the SWLS. These results are comparable with results from previous studies. Meeting the study’s objective to validate the scale, the results show that the Spanish version of the SWLS is a reliable and valid measure of satisfaction with life in the Mexican context.

Alzheimer’s disease (AD) is a disabling neurodegenerative disorder that leads to long-term functional and cognitive impairment and greatly reduces life expectancy. Early genetic studies focused on tracking variations in genome-wide DNA sequences discovered several polymorphisms and novel susceptibility genes associated with AD. However, despite the numerous risk factors already identified, there is still no fully satisfactory explanation for the mechanisms underlying the onset of the disease. Also, as with other complex human diseases, the causes of low heritability are unclear. Epigenetic mechanisms, in which changes in gene expression do not depend on changes in genotype, have attracted considerable attention in recent years and are key to understanding the processes that influence age-related changes and various neurological diseases. With the recent use of massive sequencing techniques, methods for studying epigenome variations in AD have also evolved tremendously, allowing the discovery of differentially expressed disease traits under different conditions and experimental settings. This is important for understanding disease development and for unlocking new potential AD therapies. In this work, we outline the genomic and epigenomic components involved in the initiation and development of AD and identify potentially effective therapeutic targets for disease control.