Neurodegenerative diseases represent a major and growing global health burden characterized by progressive neuronal dysfunction, axonal degeneration, and irreversible neural tissue loss. Increasing evidence identifies oxidative stress as one of several interacting pathogenic mechanisms in Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and several optic neuropathies. Interest has increasingly focused on the brain-retina axis, as the retina and optic nerve share structural, metabolic, and molecular features with the central nervous system and may provide accessible insights into neurodegeneration. This scoping review mapped current evidence on oxidative stress in neurodegeneration, emphasizing cranial nerve involvement, optic nerve vulnerability, retinal ganglion cell degeneration, visual dysfunction, oxidative biomarkers, and emerging therapeutic strategies. The review followed established methodological frameworks and PRISMA-ScR recommendations; no formal risk-of-bias appraisal was undertaken, consistent with scoping-review methodology. The literature shows that oxidative stress interacts with mitochondrial dysfunction, neuroinflammation, impaired mitophagy, ferroptosis, and altered bioenergetics, contributing to neuronal injury in cerebral and retinal disorders. Retinal ganglion cells appear particularly vulnerable because of their high metabolic demands and reliance on oxidative phosphorylation. Glaucoma and other optic neuropathies share molecular signatures with central neurodegenerative diseases. Retinal imaging and oxidative biomarkers show promise for diagnosis, monitoring, and stratification. The evidence base is nonetheless dominated by preclinical work; biomarker performance is inconsistent across matrices and assay platforms and most antioxidant clinical trials have been negative. Oxidative stress is therefore best regarded as one interacting node of a broader pathogenic network rather than a universal or predominant driver and the brain-retina continuum as a mechanistically plausible but not yet clinically validated framework for biomarker-guided neuroprotection.

Background: Determining loss of consciousness during slaughter in calves is fundamentally a neurobiological challenge requiring distinction between cortical awareness and subcortical reflex activity. Electroencephalography (EEG) and evoked potentials directly assess cortical responsiveness, while cerebral blood flow (CBF) constitutes the upstream physiological determinant of cortical viability. Aim: To synthesize current evidence on neurologic effects of slaughter modalities in calves, integrating electrophysiological and cerebral perfusion data within a mechanistic framework relevant to welfare monitoring and policy. Methods: A structured narrative review was conducted following SANRA principles. PubMed/MEDLINE was searched from inception to January 2026 using combinations of terms related to calves, cattle, EEG, evoked potentials, cerebral blood flow, stunning, and exsanguination. Inclusion was limited to peer-reviewed, PubMed-indexed studies reporting neurophysiologic endpoints in cattle or calves. EFSA scientific opinions were consulted for contextual interpretation. Results: Effective penetrating captive bolt and appropriately applied electrical stunning produce cortical lesions compatible with rapid unconsciousness. Exsanguination without prior stunning induces rapidly progressive cerebral hypoperfusion leading to cortical failure typically within seconds, with measurable inter-individual variability. Animal-based measures (ABMs) demonstrate imperfect concordance with cortical endpoints. Integration of EEG with perfusion metrics would provide a physiologically coherent method to distinguish concussive suppression, post-ictal states, and ischemic cortical failure. Conclusions: EEG and evoked potentials remain the strongest markers of cortical unconsciousness in calves. Complementary assessment of CBF can reduce interpretive uncertainty and enhance welfare monitoring precision.

Regenerative medicine has emerged as a transformative paradigm in contemporary healthcare, shifting the therapeutic focus from symptomatic management toward the restoration of tissue structure and function through biologically active interventions. Within this framework, adipose-derived products have attracted substantial interest owing to their relative abundance, ease of harvesting, and rich cellular and paracrine composition, including mesenchymal stromal cells, pericytes, and bioactive mediators with immunomodulatory potential. Among these technologies, Lipogems® represents an innovative approach based on minimally manipulated microfragmented adipose tissue, because it preserves the native stromal vascular niche and extracellular matrix architecture while avoiding enzymatic processing. This characteristic not only maintains biological integrity but also facilitates regulatory compliance in multiple jurisdictions. This narrative review provides a comprehensive synthesis of the current evidence on Lipogems®, integrating biological rationale, mechanistic insights, and clinical applications across musculoskeletal disorders and chronic pain conditions. Particular attention is devoted to its capacity to modulate inflammatory pathways, promote angiogenesis, and support tissue regeneration within complex pathological environments. In addition, the review critically appraises the methodological limitations of existing clinical studies, including heterogeneity of design and limited high-quality randomized evidence. Finally, future perspectives are explored, emphasizing the integration of precision medicine approaches, biomarker-driven patient stratification, and combinatorial regenerative strategies aimed at optimizing therapeutic outcomes.

Neurodegenerative diseases represent a major and growing global health burden characterized by progressive neuronal dysfunction, axonal degeneration, and irreversible neural tissue loss. Increasing evidence identifies oxidative stress as a central pathogenic mechanism in Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and several optic neuropathies. Interest has increasingly focused on the brain-retina axis, as the retina and optic nerve share structural, metabolic, and molecular features with the central nervous system and may provide accessible insights into neurodegeneration.This scoping review mapped current evidence on oxidative stress in neurodegeneration, emphasizing cranial nerve involvement, optic nerve vulnerability, retinal ganglion cell degeneration, visual dysfunction, oxidative biomarkers, and emerging therapeutic strategies. The review followed established methodological frameworks and PRISMA-ScR recommendations.The literature shows that oxidative stress interacts with mitochondrial dysfunction, neuroinflammation, impaired mitophagy, ferroptosis, and altered bioenergetics, contributing to neuronal injury in cerebral and retinal disorders. Retinal ganglion cells appear particularly vulnerable because of their high metabolic demands and reliance on oxidative phosphorylation. Glaucoma and other optic neuropathies share molecular signatures with central neurodegenerative diseases. Retinal imaging and oxidative biomarkers show promise for diagnosis, monitoring, and stratification. Overall, oxidative stress emerges as a convergent mechanism across the brain-retina continuum, supporting biomarker-driven neuroprotection and precision medicine.

Regenerative medicine has emerged as a transformative paradigm in contemporary healthcare, shifting the therapeutic focus from symptomatic management toward the restoration of tissue structure and function through biologically active interventions. Within this framework, adipose-derived products have attracted substantial interest owing to their relative abundance, ease of harvesting, and rich cellular and paracrine composition, including mesenchymal stromal cells, pericytes, and bioactive mediators with immunomodulatory potential. Among these technologies, microfragmented adipose tissue (MFAT) constitutes an innovative, minimally manipulated approach because it preserves the native stromal vascular niche and extracellular matrix architecture while avoiding enzymatic processing. This characteristic not only maintains biological integrity but also facilitates regulatory compliance in multiple jurisdictions. This narrative review provides a comprehensive synthesis of the current evidence on microfragmented adipose tissue in pain management, integrating biological rationale, mechanistic insights, and clinical applications across musculoskeletal disorders and chronic pain conditions. Particular attention is devoted to its capacity to modulate inflammatory pathways, promote angiogenesis, and support tissue regeneration within complex pathological environments. In addition, the review critically appraises the methodological limitations of existing clinical studies, including heterogeneity of design and limited high-quality randomized evidence. Finally, future perspectives are explored, emphasizing the integration of precision medicine approaches, biomarker-driven patient stratification, and combinatorial regenerative strategies to optimize therapeutic outcomes.

Background: Sleep and epilepsy are linked through a complex, bidirectional relationship in which physiological sleep processes influence cortical excitability and seizure susceptibility, while epileptic activity and its treatments profoundly affect sleep architecture and quality. Sleep disturbances (including insomnia, obstructive sleep apnea, circadian rhythm disorders, excessive daytime sleepiness, and fragmented sleep) are highly prevalent among people with epilepsy and contribute to impaired seizure control, cognitive dysfunction, psychiatric comorbidities, reduced quality of life, and increased healthcare utilization. Although substantial research has examined individual aspects of this relationship, the evidence remains fragmented across multiple disciplines, limiting its translation into comprehensive clinical practice.Objective: This scoping review aimed to systematically map the contemporary evidence regarding the role of sleep across the epilepsy care continuum, encompassing pathophysiological mechanisms, clinical assessment, diagnostic strategies, therapeutic interventions, digital health technologies, and emerging research priorities, while identifying critical knowledge gaps to guide future investigation and precision medicine approaches. Methods: This scoping review was conducted according to the methodological framework proposed by Arksey and O'Malley, refined by Levac and colleagues, and further finalized by the Joanna Briggs Institute, and was reported in accordance with the PRISMA Extension for Scoping Reviews (PRISMA-ScR). Comprehensive searches of PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library identified English-language studies published from January 2020 onward. Eligible publications included adults and children with epilepsy or seizure disorders addressing at least one sleep-related domain. Evidence was descriptively synthesized across predefined domains, including sleep physiology and epileptogenesis; sleep disorders and epilepsy; effects of antiseizure medications on sleep; sleep deprivation and seizure risk; diagnostic modalities, including polysomnography, electroencephalography, actigraphy, and wearable technologies; digital health and artificial intelligence; therapeutic interventions; perioperative and long-term follow-up; implementation challenges; and health equity. Conclusions: By providing the first comprehensive mapping of sleep throughout the epilepsy care continuum, this review establishes an integrated conceptual framework linking mechanistic, diagnostic, therapeutic, and technological advances. The findings highlight priorities for multidisciplinary research, support the implementation of precision sleep medicine in epilepsy, and inform future evidence-based clinical strategies designed to optimize seizure control, neurological outcomes, and patient-centered care.