Serum sickness-like reaction (SSLR) is a rare immune-mediated condition that typically affects the skin and joints after exposure to certain drugs, infections, or vaccines. Although it shares clinical similarities with serum sickness (SS), SSLR differs in its underlying mechanisms, histopathology, and causes. Despite its generally benign and self-limiting nature, SSLR is frequently misdiagnosed and may lead to unnecessary hospitalization. This narrative review summarizes current knowledge on epidemiology, pathophysiology, clinical features, diagnosis, treatment, and long-term considerations related to SSLR. The condition is most often associated with antibiotics, monoclonal antibodies, and vaccines, particularly in pediatric populations. Its pathogenesis remains incompletely understood, but proposed mechanisms include immune complex formation, altered drug metabolism, lymphocyte toxicity, and the development of anti-drug antibodies. Diagnosis is primarily clinical, although novel diagnostic tools are emerging. Management involves discontinuation of the offending agent and supportive care, such as antihistamines or nonsteroidal anti-inflammatory drugs (NSAIDs) in mild cases, and corticosteroids in more severe cases. Long-term management, especially in cases requiring potential re-exposure to the causative agent, remains challenging. Skin testing and graded oral challenges appear promising within a structured clinical framework. Increased awareness of SSLR is essential for timely recognition and appropriate care, and further research is needed to elucidate its mechanisms and inform evidence-based management strategies.

Adult hippocampal neurogenesis (AHN) is a dynamic process that sustains neural plasticity and contributes to cognition, emotion, and stress resilience. While its functional significance in humans remains debated, growing evidence suggests that AHN plays an important role in health and disease. In this review, we summarize intrinsic and extrinsic factors that modulate AHN, with particular emphasis on hormones, behavior, diet, and their impact along the hippocampal dorsoventral axis, where baseline neurogenesis is higher dorsally, but ventral neurogenesis exhibits greater plasticity and sensitivity to modulatory systems. We highlight how cognitive stimulation, physical activity, and rewarding experiences preferentially enhance dorsal hippocampal neurogenesis, whereas chronic stress and glucocorticoids mainly impair neurogenesis in the ventral hippocampus. Nutritional influences such as caloric restriction, high-fat diets, vitamins, and polyphenols are also considered, with evidence for region-specific effects. We further examine the relevance of AHN alterations in neuropsychiatric diseases, such as major depressive disorder, schizophrenia, Alzheimer’s disease, and addiction, highlighting both common mechanisms and disorder-specific vulnerabilities. Collectively, current findings suggest that AHN serves as a converging pathway connecting lifestyle, neuroendocrine regulation, and psychiatric or neurodegenerative disease. Recognizing the dorsoventral specialization of AHN could refine mechanistic models of brain function and inform the development of targeted and distinct therapeutic strategies for cognitive and affective diseases.