From the perspective of emerging adulthood, we investigated the role of culture and sex in associations between uncertainty and distress in identity development, psychological symptoms, and functioning at university among students in Canada, Spain, and Ecuador. The countries were categorized as individualistic or collectivistic according to Hofstede’s cultural dimensions. Participants included 661 students (median = 18 years, 76.6% female) in Canada (51.6%), Spain (16.2%), and Ecuador (32.2%). They completed the Identity Distress Scale, College Assessment of Psychological Problems Scale, and Student Adjustment to College Questionnaire with online surveys. Spanish students reported the greatest identity distress. Elevated academic adjustment was found for Ecuadorian students, who along with Spanish students exceeded those in Canada on social adjustment. Psychological symptoms mediated linkages between identity distress and academic and social adjustment for Canadian and Spanish women. Conversely, mediation was supported for the personal-emotional functioning of all students. Unexpected differences were found between males and females for identity distress and psychological difficulties among students in the individualistic countries. The findings underscore the need for the attention of researchers and counselors to potential variations in culture, sex, and other relevant personal and contextual factors and how they influence the identity development and well-being of university students worldwide.
Neural stem cells (NSCs) are crucial for neurogenesis in the mammalian brain, supporting the generation of neurons and glial cells during both development and adulthood. However, aging—driven by factors such as reduced growth factors, heightened inflammation, oxidative stress, and epigenetic modifications—leads to a decline in NSC activity, which is closely associated with cognitive decline. This article explores the significant reduction in neurogenesis observed in Alzheimer’s disease (AD), where amyloid-beta (Aβ) accumulation, tau pathology, mitochondrial dysfunction, and chronic neuroinflammation disrupt NSC function in the hippocampus and subventricular zone (SVZ). These disruptions impair NSC proliferation, differentiation, and migration, contributing to the progression of cognitive deficits. Additionally, this article examines experimental studies suggesting that deficits in neurogenesis often precede amyloid plaque formation in animal models, positioning impaired neurogenesis as a potential early biomarker for AD. Therapeutic strategies targeting neurogenesis, epigenetics, and inflammation—such as anti-inflammatory treatments, environmental enrichment, and modulation of systemic factors—hold promise for reversing neurogenic deficits and enhancing cognitive function. Furthermore, this article discusses both pharmacological agents and non-pharmacological strategies that show potential in promoting neurogenesis, though further research is needed to evaluate their safety and efficacy. The decline of NSC is driven by many interconnected factors, making it challenging to understand and address fully. This highlights the need for ongoing research.
