Oxidative stress (OS) is an established hallmark of cancer and neurodegenerative disorders (NDDs), which contributes to genomic instability and neuronal loss. This review explores the contrasting role of OS in cancer stem cells (CSCs) and NDDs. Elevated levels of reactive oxygen species (ROS) contribute to genomic instability and promote tumor initiation and progression in CSCs, while in NDDs such as Alzheimer’s and Parkinson’s disease, OS accelerates neuronal death and impairs cellular repair mechanisms. Both scenarios involve disruption of the delicate balance between pro-oxidant and antioxidant systems, which leads to chronic oxidative stress. Notably, CSCs and neurons display alterations in redox-sensitive signaling pathways, including Nrf2 and NF-κB, which influence cell survival, proliferation, and differentiation. Mitochondrial dynamics further illustrate these differences: enhanced function in CSCs supports adaptability and survival, whereas impairments in neurons heighten vulnerability. Understanding these common mechanisms of OS-induced redox imbalance may provide insights for developing interventions, addressing aging hallmarks, and potentially mitigating or preventing both cancer and NDDs.

Neurodegeneration and cancer are fundamentally distinct disorders: one signifies gradual neuronal loss while the latter signifies uncontrolled cell growth and survival. However, emerging evidence explores an inverse association between these conditions, suggesting that they do not arise from independent biological processes. Understanding the context-dependent behaviour of major pathways (for example, p53, PI3K/AKT/mTOR, Wnt, and immune–stress signaling) remains pivotal in elucidating the relationship between these two diseases. Pathways promoting early-life fitness, tissue repair, and tumor suppression in dividing cells can become detrimental later in life for post-mitotic neurons. Cross-species genomics studies reveal how evolution has repeatedly adapted these shared networks to balance cancer resistance with survival. Research on species exhibiting exceptional longevity and disease resistance, including naked mole rats and bowhead whales, shows that cancer resistance and longevity are not fixed traits but rather are controlled by precise regulatory mechanisms. In this review, we integrate insights from broad species genomics and multi-omic and single-cell studies to understand how evolutionarily conserved molecular crosstalks diverge at the interface of cancer and neurodegeneration.

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory diseases resulting from complex interactions between host genetics, environmental factors, immune dysregulation, and the gut microbiome. Among environmental exposures, antibiotics have emerged as important factors of IBD risk and disease course because of their profound effects on intestinal microbial communities. This review synthesizes current evidence on the class-specific effects of antibiotics on IBD, integrating epidemiological, mechanistic, and clinical studies to examine how different antibiotic classes influence disease susceptibility, progression, and microbiome recovery. Current evidence indicates that antibiotic-associated IBD risk varies according to antibiotic class, cumulative exposure, age at exposure, and antimicrobial spectrum, with broad-spectrum and anti-anaerobic agents showing the strongest associations. Mechanistically, antibiotics promote dysbiosis by depleting beneficial commensal bacteria, disrupting microbial metabolite production, expanding pathobionts and the intestinal resistome, and impairing epithelial barrier integrity and immune homeostasis. The review also discusses microbiome-preserving and microbiome-restorative approaches, including antimicrobial stewardship, fecal microbiota transplantation, prebiotics, probiotics, synbiotics, postbiotics, and dietary interventions, as potential strategies to mitigate antibiotic-associated dysbiosis. Overall, the evidence highlights the class-specific effects of antibiotics in IBD and underscores the importance of microbiome-informed antimicrobial stewardship and precision therapeutic strategies to optimize patient outcomes while minimizing long-term disruptions of host–microbiome homeostasis.

Alzheimer’s disease (AD) is a complex neurodegenerative disorder with limited effective therapies. In this study, a series of 2-(arylamino)thiazol-4(5H)-one derivatives was synthesized using an efficient microwave-assisted protocol, and evaluated for neuroprotective effects against 6-hydroxydopamine (6-OHDA)-induced oxidative stress (OS) in SH-SY5Y neuronal cells and an Aβ42-expressing Drosophila melanogaster model of AD. Among the synthesized compounds, 3n, 3i, and 3b exhibited low cytotoxicity and significant neuroprotection, as evidenced by increased cell viability, reduced reactive oxygen species (ROS) production, and preserved mitochondrial membrane potential. Notably, compound 3n demonstrated the highest activity and effectively ameliorated Aβ42-induced behavioral deficits in vivo. Molecular docking studies predicted favorable binding affinity within the acetylcholinesterase (AChE) active site, with the thiazol scaffold and aryl substituents stabilizing ligand binding through π–π stacking and hydrophobic interactions; compound 3n also formed additional hydrogen bonds enhancing its affinity. Consistent with the docking predictions, in vitro AChE inhibition studies demonstrated that compounds 3n, 3i, and 3b inhibited AChE in a concentration-dependent manner. Network pharmacology predicted seven potential core targets implicated in AD pathogenesis and related pathways, including OS, neuroinflammation, and synaptic dysfunction. Furthermore, in silico pharmacokinetic analysis indicated compliance with Lipinski’s and Veber’s rules, supporting favorable drug-like properties. While further experimental validation is essential, these findings highlight 2-(arylamino)thiazol-4(5H)-one derivatives, particularly compound 3n, as promising multifunctional candidates for further preclinical development against AD.

The clinical paradigm distinguishing chronic atopic dermatitis (AD) from acute bacterial infections is established by the emerging evidence which focuses on persistent innate immune memory as a central pathobiological factor mediating inflammatory skin diseases. While AD is classically defined by genetic susceptibility and epidermal barrier failure, progression of deep dermal Staphylococcus aureus invasion, which is characteristic of bacterial infections like cellulitis, implies a significant acute infectious condition resulting in significant tissue damage, which drives extensive innate immune reprogramming. Recent studies have established a bidirectional relationship between these conditions, yet the underlying molecular mechanisms remain undefined. However, trained immunity, governed by epigenetic and metabolic reprogramming, has now emerged as a critical mediator of this interaction. This review attempts to explore the molecular foundations of trained immunity as a mechanistic link between acute infectious conditions and chronic skin inflammation. The critical involvement of bacterial virulence factors and pattern recognition receptor signalling pathways, which instigate persistent innate memory, predisposes the tissue to recurrent infections and aggravated inflammatory responses. Furthermore, the persistent involvement of innate immune reprogramming in facilitating a mechanistic continuum between cellulitis and chronic dysregulation, characteristic of atopic dermatitis, is discussed. In continuum, we propose emphasising emerging therapeutic strategies targeting epigenetic checkpoints and metabolic rewiring to develop novel immunomodulatory interventions to combat infectious and inflammatory skin disorders.