Neurological disorders are the second cause of death and the leading cause of disability worldwide. Unfortunately, no cure exists for these disorders, but the actual therapies are only able to ameliorate people’s quality of life. Thus, there is an urgent need to test potential therapeutic approaches. Brain organoids are a possible valuable tool in the study of the brain, due to their ability to reproduce different brain regions and maturation stages; they can be used also as a tool for disease modelling and target identification of neurological disorders. Recently, brain organoids have been used in drug-screening processes, even if there are several limitations to overcome. This review focuses on the description of brain organoid development and drug-screening processes, discussing the advantages, challenges, and limitations of the use of organoids in modeling neurological diseases. We also highlighted the potential of testing novel therapeutic approaches. Finally, we examine the challenges and future directions to improve the drug-screening process.

Aging is a complex, universal biological process characterized by the progressive and irreversible decline of physiological functions across multiple organ systems. This deterioration is primarily driven by cumulative cellular damage arising from both intrinsic and extrinsic stressors. The free radical theory of aging, first proposed by Denham Harman in 1956, highlights the role of reactive oxygen species (ROS), byproducts of normal metabolism, in driving oxidative stress and age-related degeneration. Emerging evidence emphasizes the importance of redox imbalance in the onset of neurodegenerative diseases and aging. Among the critical cellular defenses against oxidative stress are sulfur-containing amino acids, namely cysteine (Cys) and selenocysteine (Sec). Cysteine serves as a precursor for glutathione (GSH), a central intracellular antioxidant, while selenocysteine is incorporated into key antioxidant enzymes such as glutathione peroxidases (GPx) and thioredoxin reductases (TrxR). These molecules play pivotal roles in neutralizing ROS and maintaining redox homeostasis. This review aims to provide an updated and critical overview of the role of thiol-containing amino acids, specifically cysteine and selenocysteine, in the regulation of redox homeostasis during aging.

Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory nervous system and affects 7–10% of the worldwide population. Neuropathic pain can be induced by the use of drugs, including taxanes, thus triggering chemotherapy-induced neuropathic pain or as consequence of metabolic disorders such as diabetes. Neuropathic pain is most often a chronic condition, and can be associated with anxiety and depression; thus, it negatively impacts quality of life. Several pharmacologic approaches exist; however, they can lead numerous adverse effects. From this perspective, the use of nutraceuticals and diet supplements can be helpful in relieve neuropathic pain and related symptoms. In this review, we discuss how diet can radically affect peripheral neuropathy, and we focus on the potential approaches to ameliorate this condition, such as the use of numerous nutritional supplements or probiotics.

The complexity of stroke pathophysiology, involving intricate neurovascular interactions and dynamic cellular responses, has long challenged the development of effective preclinical models. Traditional 2D cultures and animal models often fail to fully recapitulate human-specific features, limiting translational success. Emerging 3D systems, particularly brain assembloids and organ-on-a-chip platforms, are offering new opportunities to create more physiologically relevant stroke models. Assembloids, which integrate multiple brain-region-specific organoids, enable the study of interregional connectivity and complex cellular responses under ischemic conditions. Organ-on-a-chip platforms, by mimicking key tissue interfaces such as the blood–brain barrier and incorporating controlled fluid dynamics, enable a dynamic and highly customizable microenvironment with real-time monitoring capabilities. This review introduces and characterizes these two cutting-edge platforms (assembloids and organ-on-chip technologies), exploring their potential in stroke research while also discussing current challenges that need to be addressed for their broader adoption in translational applications.

Bruton Tyrosine Kinase (BTK) has emerged as a critical mediator in the pathophysiology of neuroinflammation associated with neurodegenerative diseases. BTK, a non-receptor tyrosine kinase predominantly expressed in cells of the hematopoietic lineage, modulates B-cell receptor signaling and innate immune responses, including microglial activation. Recent evidence implicates aberrant BTK signaling in the exacerbation of neuroinflammatory cascades contributing to neuronal damage in disorders such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, ischemic stroke, and Huntington’s disease. Pharmacological inhibition of BTK has shown promise in attenuating microglial-mediated neurotoxicity, reducing pro-inflammatory cytokine release, and promoting neuroprotection in preclinical models. BTK inhibitors, originally developed for hematological malignancies, demonstrate favorable blood–brain barrier penetration and immunomodulatory effects relevant to central nervous system pathology. This therapeutic approach may counteract detrimental neuroimmune interactions without broadly suppressing systemic immunity, thus preserving host defense. Ongoing clinical trials are evaluating the safety and efficacy of BTK inhibitors in patients with neurodegenerative conditions, with preliminary results indicating potential benefits in slowing disease progression and improving neurological outcomes. This review consolidates current knowledge on BTK signaling in neurodegeneration and highlights the rationale for BTK inhibition as a novel, targeted therapeutic strategy to modulate neuroinflammation and mitigate neurodegenerative processes.