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Anti‐aging research has made significant strides in identifying treatments capable of extending lifespan across a range of organisms, from simple invertebrates to mammals. This review showcases the current state of anti‐aging interventions, highlighting the lifespan extensions observed in animal models through various treatments and the challenges encountered in translating these findings to humans. Despite promising results in lower organisms, the translation of anti‐aging treatments to human applications presents a considerable challenge. This discrepancy can be attributed to the increasing complexity of biological systems, species‐specific metabolic and genetic differences, and the redundancy of metabolic pathways linked to longevity. Our review focuses on analyzing these challenges, offering insights into the efficacy of anti‐aging mechanisms across species and identifying key barriers to their translation into human treatments. By synthesizing current knowledge and identifying gaps in translatability, this review aims to underscore the importance of advancing these therapies for human benefit. Bridging this gap is essential to assess the potential of such treatments in extending the human healthspan. [ABSTRACT FROM AUTHOR]

Two of the most common and incapacitating mental health disorders around the world are major depressive disorder (MDD) and post-stroke depression (PSD). MDD is thought to result from abnormal connectivity between the monoaminergic, glutamatergic, GABAergic, and/or cholinergic pathways. Additional factors include the roles of hormonal, immune, ageing, as well as the influence of cellular, molecular, and epigenetics in the development of mood disorders. This complexity of factors has been anticipated by the Swiss psychiatrists Paul Kielholz and Jules Angst who introduced a multimodal treatment of MDD. Depression is the predominant mood disorder, impacting around one-third of individuals who have experienced a stroke. MDD and PSD share common underlying biological mechanisms related to the disruption of monoaminergic pathways. The major contributor to PSD is the stroke lesion location, which can involve the disruption of the serotoninergic, dopaminergic, glutamatergic, GABAergic, or cholinergic pathways. Additionally, various other disorders such as mania, bipolar disorder, anxiety disorder, and apathy might occur post-stroke, although their prevalence is considerably lower. However, there are differences in the onset of MDD among mood disorders. Some mood disorders develop gradually and can persist for a lifetime, potentially culminating in suicide. In contrast, PSD has a rapid onset because of the severe disruption of neural pathways essential for mood behavior caused by the lesion. However, PSD might also spontaneously resolve several months after a stroke, though it is associated with higher mortality. This review also provides a brief overview of the treatments currently available in medical practice. • The interplay between genes and the environment in the development of mood disorders • The influence of immune, hormonal, and epigenetic environment in the development of affective disorders. • Similarities and differences between molecular mechanisms underlying MDD and PSD • The treatments currently available in medical practice [ABSTRACT FROM AUTHOR]