Psychological support and postpartum depression in twin gestations: a prospective analysis using the Edinburgh Scale.

Genetic frontotemporal dementia (FTD) encompasses a spectrum of heterogeneous neurodegenerative disorders, most commonly caused by an autosomal dominant mutations in the chromosome 9 open reading frame 72 (), progranulin () or microtubule associated protein tau () genes. Despite shared genetic origins, affected individuals often display substantial variability in age at onset and disease progression, even within the same mutation or family. Understanding the determinants of this variability could help identify potential targets for intervention, either to delay symptom onset in individuals or to slow disease progression in symptomatic patients. In this context, cognitive reserve has emerged as a key framework for understanding heterogeneity in cognitive ageing, including FTD. Cognitive reserve refers to the ability to maintain cognitive function despite neuropathological damage, a concept used to explain heterogeneity in clinical outcomes among individuals with similar levels of brain pathology. Certain modifiable factors, most notably educational and occupational attainment, have been shown to enhance the capability to maintain cognitive performance relatively well in ageing and disease. Other factors, including sex and socio-environmental context, may also contribute to cognitive reserve. In this regard, it has been reported that females with genetic and sporadic FTD present higher cognitive reserve than males, suggesting that sex modulates resilience to frontotemporal neurodegeneration. Additionally, neighbourhood disadvantage has been associated with reduced cognitive reserve, but the role played by country or region of residence, which may reflect diverse cultural, social and environmental contexts, has never been explored in large multinational FTD cohorts. Although these studies offer preliminary insights, a comprehensive evaluation of multiple modifiable and non-modifiable predictors, and their interactions, across the full disease course, from the presymptomatic to symptomatic disease stages, has never been conducted.