Search Results (1,592)

Background/Objectives: Lipidomics has become a key component of systems biology, enabling comprehensive characterisation of lipid species and their roles in health and disease. As regulators of membrane architecture, energy balance, inflammation, and cellular signalling, lipids offer a powerful framework for understanding metabolic dysfunction. In veterinary medicine, however, lipidomics remains comparatively underdeveloped. In cats, lipid metabolism is central to disorders such as hepatic lipidosis, cystitis, obesity, diabetes mellitus, and chronic inflammatory enteropathies, yet available data remain limited. This systematic review synthesised current evidence on lipidomics and lipid-focused profiling in feline disease and identified lipid alterations with potential clinical relevance. Methods: Following PRISMA 2020 guidelines, PubMed, ScienceDirect, and Scopus were searched for original studies (1994–2026) evaluating lipidomics or lipid-focused profiling in cats. Eligible studies assessed lipid species, fatty acids, lipid mediators, or lipoproteins in disease or physiological states. Owing to methodological heterogeneity, findings were synthesised narratively. Results: Seventeen studies met inclusion criteria, covering hepatic, urinary, gastrointestinal, renal, neurological, oncological, metabolic, and pharmacologically modulated conditions. Recurring alterations involved lipoproteins, triglycerides, phospholipids, sphingolipids, fatty acids, and oxylipins. More consistent patterns emerged in hepatic lipidosis, where lipoprotein disturbances may aid diagnosis; in lower urinary tract disease, where PUFA-derived oxylipins differentiated bacterial from idiopathic cystitis; and in obesity, where phospholipid and triglyceride shifts reflected metabolic risk. Fatty acid remodelling in chronic enteropathies aligned with mucosal inflammation, while sphingolipid changes in neurological disease correlated with severity. Heterogeneity in analytical platforms, dietary control, and study design limited comparability. Conclusions: Feline lipidomics reveals biologically meaningful alterations with emerging diagnostic and prognostic value. Although still developing, lipid-focused approaches may enhance disease characterisation and support translational research. Larger, standardised studies and robust reference datasets are needed to validate lipid signatures for clinical implementation. Full article

The global rise in cognitive decline and neurodegenerative disorders has intensified the search for safe and accessible strategies to support brain health. In recent years, nutraceuticals have gained considerable attention as potential modulators of neurological function due to their antioxidant, anti-inflammatory, and neuroprotective properties. Increasing evidence suggests that oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired neurovascular integrity play central roles in the pathogenesis of several neurodegenerative diseases, namely Alzheimer’s, Parkinson’s disease and autism spectrum disorder, among others. This narrative review provides an integrated overview of selected nutraceuticals with potential relevance to brain-related disorders, including biotin, folinic acid, flavonoids (apigenin, diosmin, luteolin, naringin, pycnogenol, and quercetin), huperzine A, Lion’s mane, olive oil polyphenols, oleuropein and palmitoylethanolamide. Rather than presenting a purely descriptive summary, we considered both mechanistic and clinical evidence, highlighting differences in the strength, consistency, and quality of available data across compounds. Among the reviewed compounds, huperzine A, specific flavonoids—particularly luteolin—and olive oil polyphenols demonstrated relatively stronger and more consistent support across experimental models and emerging clinical studies, mainly through modulation of cholinergic signaling, neuroinflammatory pathways, and oxidative stress responses. In contrast, evidence for other agents remains limited, heterogeneous, or primarily at the preclinical level. Overall, this review aims to provide a clearer and more structured synthesis of the current literature on neuronutrition, identifying compounds with the most promising profiles while outlining key limitations and research gaps that need to be addressed to better define their role in brain health. Full article

Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection and is frequently complicated by sepsis-associated encephalopathy (SAE), which contributes to long-term cognitive and neuropsychiatric sequelae. Despite advances in critical care, effective targeted therapies for SAE remain limited. Aquaporin-4 (AQP4), the predominant astrocytic water channel, plays a central role in cerebral water homeostasis, neuroinflammatory signaling, and blood–brain barrier integrity, suggesting its potential involvement in sepsis-induced cerebral dysfunction and neurorepair processes. Polymicrobial sepsis was induced in C57BL/6J mice using the cecal ligation and puncture (CLP) model. AQP4 activity was pharmacologically modulated through either inhibition or facilitation following sepsis induction. Disease severity was assessed using physiological parameters and a modified murine sepsis score. Neurological outcomes were evaluated through standardized behavioral tests assessing locomotor activity, motor coordination, cognitive performance, and depressive-like behavior. Neuroinflammatory and neuronal changes were examined by immunohistochemical analyses of microglial activation (Iba1), astroglial reactivity (GFAP), neuronal integrity (NeuN), and AQP4 expression. Compared with AQP4 facilitation, pharmacological inhibition of AQP4 was associated with a more favorable clinical recovery profile, reflected by lower sepsis severity scores and a more favorable body weight trajectory during the recovery phase. Behavioral analyses demonstrated preserved cognitive function, enhanced motor coordination, and reduced depressive-like behavior in AQP4 inhibitor-treated mice compared with animals receiving AQP4 facilitation. At the histological level, the inhibitor-treated group showed lower microglial and astroglial activation and better preservation of neuronal markers than the facilitator-treated group, whereas AQP4 facilitation exacerbated neuroinflammatory responses and neuronal alterations. These findings highlight a dual, context-dependent role of AQP4 in sepsis-associated cerebral dysfunction. These findings suggest that AQP4 modulation influences sepsis-associated cerebral dysfunction in a context-dependent manner. Within our experimental design, AQP4 facilitation was associated with worse outcomes, whereas AQP4 inhibition was associated with a comparatively more favorable neurobehavioral and histological profile. Full article

Recreational (“party”) drug use is prevalent in social environments and is increasingly relevant in ophthalmic care. While the neurological and cardiovascular consequences of these subokstances are well documented, their ocular and visual effects may not be fully recognized or consistently reported in clinical practice. This invited narrative review summarizes clinical observations and translational mechanisms underlying ophthalmic manifestations associated with commonly used recreational substances, including sympathomimetic stimulants (cocaine, amphetamines), empathogens (3,4-methylenedioxymethamphetamine (MDMA), inhalants (alkyl nitrites, “poppers”), and cannabinoids (cannabis/Δ9-tetrahydrocannabinol (THC)). Particular focus is placed on vascular dysregulation, altered ocular perfusion pressure, venous outflow impairment, oxidative stress, and neuro-ophthalmic dysfunction. Characteristic presentations, diagnostic pitfalls, and management considerations are discussed. Improved awareness of drug-related ocular effects may facilitate earlier recognition of such conditions and help reduce the risk of visual complications. Other recreational substances, including hallucinogens and emerging psychoactive compounds, may also have ocular effects, although current evidence remains limited. Full article

Wearable sensors enable continuous recording of electrocardiographic, photoplethysmographic, and inertial signals and have accelerated the development of digital biomarkers in cardiovascular medicine. Transthyretin amyloidosis (ATTR) is a progressive multisystem disease characterized by arrhythmia, conduction disturbances, hemodynamic impairment, autonomic dysfunction, and gait abnormalities, making it theoretically suitable for multimodal wearable monitoring. This review summarizes current knowledge on wearable applications in amyloidosis with ATTR serving as an illustrative case, evaluates the plausibility of extrapolating signal-based biomarkers from related cardiovascular and neurological cohorts, and outlines methodological and implementation challenges. ATTR-specific data remain limited to small observational studies, mainly on long-term rhythm monitoring and supervised functional assessment. More comprehensive findings support the extraction of metrics such as atrial fibrillation burden, activity patterns, gait variability, and heart rate variability. However, ATTR-related structural remodeling and high arrhythmia burden may distort conventional digital biomarkers, necessitating disease-specific preprocessing and prospective validation. Wearable monitoring in ATTR is technically feasible and biologically plausible but remains investigational. Before routine integration into care pathways can be recommended, standardized, phenotype-stratified studies are needed that link wearable-derived characteristics to assessed clinical outcomes. Full article

Objective. The aim of this study was to evaluate clinical characteristics, surgical outcomes, and factors influencing postoperative neurological status in patients undergoing resection of intradural spinal tumors, with particular emphasis on the role of preoperative neurological function and intraoperative neuromonitoring (IONM). Methods. We conducted a retrospective analysis of 108 patients who underwent surgical resection of intradural spinal tumors at a single neurosurgical center. Patients were categorized into intradural extramedullary (IDEM) and intramedullary (IM) tumor groups. The primary endpoint was the occurrence of a new or worsened postoperative motor deficit at discharge. Secondary endpoints included postoperative sphincter dysfunction and functional status assessed using the modified McCormick scale at discharge and at 6-month follow-up. Categorical variables were compared using the Chi-square or Fisher’s exact test, and continuous variables using the Mann–Whitney U test. Results. A total of 108 patients were included (61.1% female; mean age 55.7 ± 15.6 years). IDEM tumors accounted for 77 cases, while 31 were intramedullary. There were no significant differences between IDEM and IM tumors in the rate of new or worsened postoperative motor deficits (9.1% vs. 6.7%, p = 1.000), postoperative sphincter dysfunction (2.6% vs. 0%, p = 1.000), or functional outcomes assessed using the modified McCormick scale at discharge (p = 0.85) and at 6 months (p = 0.24). Preoperative motor deficit was strongly associated with postoperative motor dysfunction in the overall cohort (86% vs. 14%, p < 0.001), with an even stronger effect observed in the IM subgroup (90.9% vs. 9.1%, p < 0.001). IONM was used in 34.3% of cases and was significantly associated with tumor location, histopathology, and surgical complexity. However, IONM use was not associated with postoperative motor outcomes (p = 0.645). Conclusions. Postoperative neurological outcomes following intradural spinal tumor resection are comparable between intramedullary and extramedullary lesions. Preoperative motor deficit is the strongest predictor of postoperative neurological status, particularly in intramedullary tumors, underscoring the importance of early surgical intervention. IONM is preferentially used in higher-risk cases and should be interpreted as a marker of surgical complexity rather than an independent determinant of outcomes. Full article

Background: Emerging evidence indicates that the liver plays a key role in spinal cord injury (SCI) pathophysiology. Method: This study reanalysed published proteomic datasets from rat models and patients with SCI using bioinformatics and literature/database searches. The aim was to identify liver-specific molecular signatures in SCI blood samples and to link these to severity and neurological recovery at various time points (acute/sub-acute and chronic). Results: Across species, a high proportion of injury severity and neurological recovery-associated proteins were linked to liver function. Notably, non-improvers exhibited prolonged sub-acute proinflammatory responses. These changes were not restricted to classical acute-phase reactants but reflected coordinated alterations in hepatic metabolic and synthetic pathways. Pathway analysis consistently highlighted Liver X Receptor /Retinoic X Receptor (LXR/RXR), complement system/cascade and DHCR24 signalling pathways, with predicted directional changes linked to recovery status. Several proteins were identified and categorised as markers of liver dysfunction, metabolic function, complement/coagulation factors and/or acute-phase proteins. Alpha-2-HS-glycoprotein (AHSG) and afamin (AFM) were commonly dysregulated across species datasets, suggesting conserved roles in inflammation and lipid metabolism. Further associations with liver pathologies such as fibrosis and cirrhosis, particularly in non-improvers, were identified. Conclusion This work builds on emerging evidence of hepatic involvement in SCI by providing cross-species, time-resolved proteomic support for altered liver-associated protein output following injury. Together, these findings underscore the central role of hepatic responses in SCI, highlighting liver-associated proteins and pathways as candidate biomarkers that may aid in stratifying recovery trajectories and informing clinical prognostication. Full article

Background/Objectives: Cardiovascular disease (CVD), particularly coronary artery disease (CAD), is increasingly linked to microvascular inflammation driven by interactions between immune, vascular, and neuroendocrine systems. Mast cells (MCs), strategically positioned near blood vessels, play pivotal roles in this process through the release of inflammatory and vasoactive mediators, contributing to increased vascular permeability, endothelial dysfunction, and tissue inflammation in conditions including ischemia–reperfusion (I/R) and CVD. This comprehensive review examines the cellular and molecular mechanisms underlying MC-mediated microvascular inflammation, with emphasis on neuroimmune regulation through the heart–brain axis, and evaluates the therapeutic potential of flavonoids. Methods: A review of in vitro, animal, and clinical studies was conducted to assess MC-mediated cardiovascular pathology and the pharmacological effects of natural flavonoids on MC activation and microvascular inflammation. Results: Psychological and physical stress activates hypothalamic corticotropin-releasing hormone (CRH) signaling, directly triggering coronary MC degranulation via CRHR-1 and CRHR-2 receptors, while co-released neuropeptides, including neurotensin and urocortin, amplify this neuroimmune cascade. Traumatic brain injury, autonomic dysregulation, and atrial fibrillation further perpetuate this bidirectional heart–brain axis, linking neurological stress to microvascular injury and adverse cardiac remodeling. An autocrine–paracrine CRH amplification loop sustains chronic coronary microvascular inflammation, contributing to heart failure with preserved ejection fraction (HFpEF) and MC activation disease (MCAD)-related cardiovascular manifestations. Natural flavonoids were found to inhibit MC activation, suppress inflammatory mediator synthesis, and protect microvascular integrity through multiple molecular targets, including calcium signaling, transcription factors, oxidative stress pathways, and CRHR-1-mediated neuroimmune signaling. Conclusions: While challenges remain regarding bioavailability and standardization, multi-compound formulations targeting multiple risk factors hold promise for preventing CVD progression. Future research directions for advancing these natural compounds toward clinical implementation are identified. Full article

Objective: Cerebral ischemia–reperfusion (I/R) injury constitutes a pivotal pathological driver in cerebrovascular disorders such as stroke, yet effective therapeutic interventions remain scarce. This study explored whether hydrogen sulfide (H₂S) mitigates endothelial cell damage in the cerebral vasculature during I/R by modulating nicotinamide phosphoribosyltransferase (NAMPT) activity and its S-sulfhydration status, consequently restoring mitochondrial integrity and energetic homeostasis. Methods: Primary cerebrovascular endothelial cells (ECs) were subjected to hypoxia/reoxygenation (H/R) conditions in vitro, while rats experienced middle cerebral artery occlusion/reperfusion (MCAO/R) in vivo. The H₂S donor sodium hydrosulfide (NaHS) was administered, and outcomes were evaluated through Western blot analysis, S-sulfhydration assays, mitochondrial functional tests, autophagy profiling, and neurobehavioral assessments. The contributions of NAMPT and S-sulfhydration were validated using FK866 and dithiothreitol (DTT), respectively. LC-MS/MS was employed to identify candidate S-sulfhydration sites on NAMPT triggered by H₂S. Results: In cellular models, NaHS substantially boosted NAMPT enzymatic activity, elevated NAD⁺ and ATP levels, and enhanced cell survival. These protective benefits were nullified upon NAMPT inhibition with FK866 or reversal of S-sulfhydration via DTT. In animal studies, NaHS treatment significantly diminished infarct volume and ameliorated neurological deficits in MCAO/R rats; however, pretreatment with FK866 or DTT attenuated these benefits. Mechanistic investigations revealed that NaHS promoted S-sulfhydration of NAMPT, thereby activating autophagy of dysfunctional mitochondria. LC-MS/MS analysis confirmed enhanced S-sulfhydration at Cys39 and Cys397 residues of NAMPT following H₂S exposure. Conclusions: H₂S exerts neuroprotection against cerebral I/R injury in rats through S-sulfhydration-mediated activation of NAMPT, which improves mitochondrial performance and stimulates autophagy in cerebrovascular ECs. Full article

Despite being distinct clinical entities, major depressive disorder (MDD) and Parkinson’s disease (PD) have some shared physiological pathways, including mitochondrial dysfunction and inflammation. Our interest was whether these common physiological mechanisms are reflected in brain activity variations as well. Therefore, this study aimed to identify common characteristics in resting-state electroencephalography (EEG) between the conditions by comparing features among patients with MDD, PD, and healthy controls. The methodology comprised two stages: analyzing differences between patients and healthy individuals and exploring consistent trends between PD and MDD, based on EEG data from PRED + CT database. Age-corrected regression analysis of five EEG features revealed PD and MDD had the following overlapping features: shared abnormalities in theta, alpha and beta relative power, as well as sample entropy in the delta (centroparietal, temporal, and parietal areas), theta (parieto-occipital), and gamma (central) bands. Furthermore, interhemispheric asymmetry was evident across all bands, especially in the frontal and centroparietal regions. When combining these findings with their directional trends (positive or negative), common EEG features included increased theta and decreased alpha-beta power, along with increased parieto-occipital and reduced gamma entropy at FCz. These findings suggest shared EEG markers between PD and MDD, supporting the potential for efficient neurological disorder diagnosis. Full article

Traumatic brain injury (TBI) is a prevalent neurological disorder that induces severe neurological dysfunction and markedly reduces quality of life owing to its complex pathophysiology and limited therapeutic options. Conventional pharmacological and surgical interventions show restricted efficacy because of poor blood–brain barrier penetration and inability to address secondary injury cascades. In recent years, hydrogels have shown significant potential for TBI repair due to their superior biocompatibility, high water content, and ability to mimic the native extracellular matrix (ECM). This review systematically examines recent advances in hydrogel applications for TBI therapy, focusing on their roles as drug delivery platforms, stem cell scaffolds, neuroregeneration promoters, inflammation modulators, and angiogenesis facilitators. Particular emphasis is placed on the therapeutic benefits and underlying mechanisms of ECM-derived hydrogels, self-assembling peptide (SAP) hydrogels, stimuli-responsive smart hydrogels, and functionalized multicomponent systems. Current challenges and limitations in hydrogel applications are also discussed, along with future research directions, to provide scientific rationale and practical guidance for precision TBI therapy. Full article

Background and Objectives: Hereditary transthyretin amyloidosis (ATTRv), a multisystemic disorder caused by transthyretin (TTR) gene mutations, exhibits phenotypic heterogeneity that can hamper recognition in non-endemic areas. Here, we investigated the clinical practice of ATTRv amyloidosis over an extended period and examined the challenges currently faced in non-endemic regions. Materials and Methods: We conducted an observational study of 18 patients with ATTRv amyloidosis diagnosed at Oita University and its affiliated hospitals between 2000 and 2025, using both retrospective and prospective data collection, to evaluate clinical features, treatments, and outcomes. Results: The median age at disease onset was 64 years, and 27.8% of patients had a family history of the disease. Val30Met (V30M) was the most common (55.6%) mutation; Tyr114Ser was the most common non-V30M variant. Sensory disturbances (50%) were the most common initial symptoms, followed by cardiac symptoms (38.9%). The cardiology department most frequently diagnosed ATTRv amyloidosis, followed by the neurology department. Two patients were relatives of previously diagnosed probands and were therefore identified during their first visit to the initial department. New diagnoses increased over time (1 in 2000–2009, 7 in 2010–2019, and 10 in 2020–2025), although diagnostic delays persisted. After the therapeutic agents shifted from patisiran to vutrisiran, the serum TTR value decreased (p = 0.0078) without significant deterioration in cardiac parameters. In the current treatment era, longer-term survivors have been observed, but multiple organ dysfunction has become more apparent, and ocular manifestations have emerged as a clinically important problem, particularly in patients with longer disease duration (p = 0.0169). Conclusions: Physicians in various departments must remain vigilant for the presence of ATTRv amyloidosis. Addressing challenges faced by long-term survivors, including ocular manifestations and central nervous system complications, has become crucial, even in non-endemic areas. Full article

Background and Objectives: The goal of this study was to evaluate the associations between peripapillary retinal nerve fibre layer (pRNFL) thickness, disability-related clinical measures, including the Expanded Disability Status Scale (EDSS), and report-based magnetic resonance imaging (MRI) findings in patients with multiple sclerosis (MS), and to explore potential longitudinal relationships between pRNFL changes and disability progression. Materials and Methods: A retrospective single-centre study was conducted in patients with MS diagnosed according to the 2010/2017 McDonald criteria at the Neurology Clinic of the Hospital of Lithuanian University of Health Sciences Kauno Klinikos. The study included 84 patients. pRNFL thickness was measured using optical coherence tomography (OCT) at baseline (defined as the time of diagnosis) and, for some patients, follow-up. Associations between pRNFL measures and clinical as well as MRI-derived variables were assessed using Spearman correlation and multivariable linear and ordinal regression analyses. Results: In cross-sectional analyses, lower baseline pRNFL thickness was associated with higher baseline disability (ρ = −0.257, p = 0.019) and greater worsening of EDSS over time (ρ = −0.268, p = 0.013). Significant associations were also observed between thinner pRNFL and pyramidal system impairment and bowel/bladder dysfunction. In adjusted linear regression models, each 20 µm reduction in pRNFL was associated with a 0.46-point increase in EDSS (B = −0.023, SE = 0.009) and a 0.32-point rise in cerebellar functional system score (B = −0.016, SE = 0.006). Among the 45 patients with repeat OCT, exploratory longitudinal pRNFL thinning showed directional trends toward increasing disability; however, these associations were not consistently significant after adjustment. Baseline pRNFL thickness showed a modest association with a composite MRI regional lesion score derived from report-based binary variables. Conclusions: In this real-world retrospective cohort, thinner pRNFL was associated with greater disability in cross-sectional analyses. Associations with individual MRI regions and radiological activity were limited and inconsistent. These findings should be interpreted as preliminary and hypothesis-generating. Further prospective studies are needed to clarify the potential role of OCT-derived pRNFL measurements. Full article

Background/Objectives: Neurological diseases are increasing worldwide, but the biological processes underlying these diseases remain poorly understood, and existing treatments have been ineffective at arresting disease progression. Emerging data indicate that dysbiosis of the microbiota–gut–brain axis and malnutrition are comorbid factors in neurological dysfunction. Methods: An extended search strategy was developed using a multifaceted approach across various databases to identify eligible studies published between January 2010 and February 2026. Results: Results showed uniform relationships among neurological conditions, loss of microbial richness, loss of short-chain fatty acid-producing bacteria, neuroinflammation, and nutritional susceptibility. The review also identifies methodological trends in microbiome profiling and nutritional assessment and suggests an integrative framework of symptom-linked microbial imbalance, malnutrition, and inflammatory processes. Conclusions: Although dietary modulation and microbiome-targeted interventions appear promising, the evidence is mostly correlational. Longitudinal and interventional studies should be well-designed to elucidate causal mechanisms and to provide effective clinical strategies. Full article

Background: The photopic negative response (PhNR) of the full-field electroretinogram is a retinal ganglion cell-weighted functional signal increasingly proposed as a clinical biomarker. Despite extensive study across ocular and systemic diseases, its precise clinical role and incremental value remain incompletely established. Methods: This narrative review synthesizes key human studies of the photopic negative response, with emphasis on physiological basis, recording methodology, and clinical contexts in which PhNR may provide added functional insight. Results: In glaucoma, PhNR provides an objective measure of retinal ganglion cell dysfunction that correlates moderately with optical coherence tomography (OCT)-derived structural loss and visual field indices, but with substantial inter-individual variability. Its greatest clinical utility lies in early disease detection, cross-sectional functional assessment, and documenting short-term functional changes following intraocular pressure reduction, rather than longitudinal progression monitoring. Beyond glaucoma, PhNR reveals inner retinal dysfunction in systemic and genetic conditions, particularly idiopathic intracranial hypertension and diabetes, where retinal ganglion cells may reflect broader neurological or metabolic stress. Conclusions: PhNR is best viewed not as a standalone diagnostic or progression tool, but as a complementary functional biomarker that adds objective insight when structural imaging or psychophysical testing is limited or discordant. Its role aligns closely with the retina’s emerging function as a mirror of systemic and genetic disease, provided recordings are standardized and results interpreted cautiously. Full article