The blood–brain barrier (BBB) is a critical structure that maintains brain homeostasis by selectively regulating nutrient influx and waste efflux. Not surprisingly, it is often compromised in neurodegenerative diseases. In addition to its involvement in these pathologies, the BBB also represents a significant challenge for drug delivery into the central nervous system. Nanoparticles (NPs) have been widely explored as drug carriers capable of overcoming this barrier and effectively transporting therapies to the brain. However, their potential to directly address and ameliorate BBB dysfunction has received limited attention. In this review, we examine how NPs enhance drug delivery across the BBB to treat neurodegenerative diseases and explore emerging strategies to restore the integrity of this vital structure.

Tumor innervation is a complex interaction between nerves and cancer cells that consists of axons invading tumors, and its complexity remains largely unknown in humans. Although some retrospective studies have provided important insights into the relationship between nerves and tumors, further knowledge is required about this biological process. Animal experiments have elucidated several molecular and cellular mechanisms of tumor innervation; however, no experimental models currently exist to study interactions between human cancer and nerve cells. Human pluripotent stem cells can differentiate into neurons for research purposes; however, the use of these neurons to study interactions with cancer cells remains largely unexplored. Hence, here we analyze the potential of human pluripotent stem cells to study the interaction of cancer cells and neurons derived from human pluripotent stem cells to unravel the poorly understood mechanisms of human tumor innervation.

Early menarche has been recognized as an early-life marker of metabolic vulnerability, yet its link to gestational diabetes mellitus (GDM) remains unclear. We investigated this association in a retrospective case–control study of 71 cases and 355 controls from a tertiary hospital in Mexico City. Age at menarche was evaluated both in categories and using restricted cubic splines to capture potential non-linear trends. Mediation analysis explored the contribution of pregestational body mass index (BMI) to the relationship between variables. Women who experienced menarche before age 12 had more than twice the odds of developing GDM compared with those whose menarche occurred between 12 and 15 years (adjusted OR = 2.51, 95% CI 1.40–4.50). In contrast, late menarche showed a minor, non-significant increase in risk. The spline models revealed a subtle U-shaped pattern, suggesting that both very early and delayed pubertal timing may carry metabolic disadvantages. The mediation analysis showed that pregestational BMI accounted for only a minor share of this association. Overall, the findings indicate that early pubertal onset may influence glucose regulation during pregnancy through pathways beyond adiposity, highlighting early menarche as a valuable marker for identifying women at higher risk of GDM.