搜索结果：Animal genetics

Methicillin-resistant Staphylococcus aureus (MRSA) is a major antimicrobial-resistant pathogen affecting both human and animal health. Although historically associated with healthcare settings, MRSA is now established in livestock production and throughout the production chain. Its detection in animals, food products, and processing environments reflects the complex ecology of antimicrobial resistance (AMR) in modern food systems. This narrative review synthesizes current evidence on the molecular basis of methicillin resistance and multidrug resistance determinants, as well as the epidemiology of MRSA in food-associated settings. Particular emphasis is placed on its occurrence in animal-derived foods and key reservoirs within farms, slaughterhouses, and processing environments. Livestock-associated populations are dominated by clonal complex CC398. In contrast, CC9 is prevalent in pig production systems in Asia, while CC5-related lineages occur at the human and animal interface. MRSA has been detected in retail meat and animal-derived foods at low but measurable prevalence, indicating contamination during slaughter and processing. Virulence determinants include staphylococcal enterotoxins linked to food poisoning and Panton-Valentine leukocidin associated with severe infections. Biofilm formation and adhesins further support persistence and colonization. Epidemiological and molecular evidence indicates that livestock, processing environments, and food-contact surfaces act as interconnected reservoirs sustaining MRSA circulation. Human exposure occurs primarily through occupational contact and environmental pathways, whereas foodborne transmission appears less common. Effective control requires integrated surveillance, responsible antimicrobial use in livestock production, and strict hygiene practices throughout the production chain within a One Health framework.

Fibromyalgia, a syndrome characterized by hyperalgesia and 'negative emotionality', and major depressive disorder (MDD) demonstrate substantial overlaps in clinical, neurobiological, and therapeutic domains. Currently, treatment options for fibromyalgia remain limited; however, the epidemiology of this syndrome continues to grow worldwide. The use of animal models is indispensable for developing new treatment strategies for fibromyalgia. Meanwhile, the choice of animal paradigms is limited. Here, we used the ultrasound exposure of emotional stress on CBA, BALB/c, and C57BL/6 mouse strains to model this condition and to identify new molecular targets of fibromyalgia treatment. We exposed young male mice of three common strains to a three-week ultrasound stress (US) comprising emotionally negative and neutral frequencies of 20-25 kHz and 25-45 kHz, resulting in the development of altered pain sensitivity and signs of 'negative emotionality'. Specifically, mice were studied for timid-like/aggressive behaviors and the tail flick response. Serum levels of corticosterone, cortisol, β-Endorphin, and brain-derived neurotrophic factor (BDNF), as well as brain gene expression of interleukin-33 (Il-33), Bdnf, and its receptor Trkb were investigated. Among the stressed mouse strains, C57BL/6 mice displayed augmented pain sensitivity, allodynia, and suppressed dominant behavior, whereas CBA and BALB/c mice demonstrated opposing changes. Glucocorticoid levels were increased in all stressed groups. Stressed C57BL/6 mice showed downregulated gene and protein expression of functionally inter-related BDNF and IL-33 molecules in the hippocampus, amygdala, and striatum, significantly correlating with behavioral outcomes, as well as lowered blood levels of β-Endorphin and elevated cortisol concentrations. Altogether, our study identified the BDNF/IL-33 regulatory pathway as a molecular correlate of fibromyalgia, and the use of US-exposed young C57BL/6 mice as a potential model that recapitulates this syndrome.

Myocardial infarction initiates complex remodeling processes involving the renin-angiotensin system, through activation of the angiotensin II type 1 receptor (AT1R). This study correlated AT1R expression with fibrosis and cardiac function in the heart and kidneys following cardiac ischemic injury in animal models. Male Sprague-Dawley rats underwent Sham surgery, Ischemia/Reperfusion (I/R, 20-min ligation) or Permanent Ligation (PL) of the left anterior descending artery. Cardiac function was assessed by echocardiography. AT1R expression was measured in the heart (infarct and remote areas) and kidneys (cortex, medulla) via [125Iodine]Sarcosine1-Isoleucine8-Angiotensin II autoradiography. Collagen deposition was evaluated through picrosirius red staining. Left ventricular (LV) ejection fraction declined in PL models but remained stable following I/R. Post-I/R, a transient increase in cardiac AT1R (day-3 to week-5) correlated with an increase in collagen, whereas after PL, elevations persisted through week-12. Infarct areas consistently displayed higher AT1R and collagen than remote areas. Renal AT1R and collagen levels were unchanged across groups. In analyses with pooled animals, cardiac AT1R expression correlated with collagen and inversely correlated with LV Fractional Shortening (LVFS), whereas LVFS inversely correlated with collagen deposition. These findings suggest that cardiac AT1R levels may serve as a target of cardiac remodeling, while changes in renal AT1R appear less pronounced.

Modified citrus pectin (MCP), a polysaccharide from citrus fruits, modulates galectin-3 (Gal-3) and immune responses. Although MCP exhibits notable immunomodulatory effects, its role in drug-induced splenic and systemic toxicity remains unexplored. This study investigated the effects of MCP modulation on splenic immune remodeling and galectin expression in a rat model of cisplatin-induced toxicity. Wistar rats were divided into four groups (n = 5 animals/group): control (SHAM), MCP (100 mg/kg/day for 7 days), cisplatin (CIS, 10 mg/kg/day for 3 days), and MCP + CIS. Spleens were collected 6 h after the final cisplatin dose. Cisplatin induced splenic structural disorganization and selectively reduced nitric oxide levels without broadly affecting antioxidant enzymes. Cisplatin treatment was associated with increased CD3⁺ T cell labeling and enhanced tissue expression of Gal-1, -3, and - 9. MCP administration did not restore splenic architecture but promoted increased hemosiderin deposition in the red pulp, suggestive of enhanced erythrophagocytosis and altered iron handling, and markedly reduced CD3⁺ T cell immunoreactivity. MCP associated with cisplatin also reduced Gal-1 and Gal-3 levels and altered the relationship between galectins and splenic immune cell populations. Correlation analyses revealed positive associations between Gal-1, -3, and - 9 and CD68⁺ macrophages, as well as a selective association between Gal-3 and CD3⁺ T cells, exclusively in MCP + CIS animals. MCP does not mitigate cisplatin-induced splenic damage but alters immune cell distribution and galectin-related responses during cisplatin exposure.

This study seeks to investigate the underlying mechanism of glycolytic key gene bisphosphoglycerate mutase (BPGM) in nonalcoholic fatty liver disease (NAFLD). qRT-PCR and immunohistochemistry were utilized to detect BPGM levels in clinical NAFLD samples. HepG2 cells and liver organoids were treated with free fatty acid. (FFA). The role of BPGM in NAFLD was explored at cellular, organoid, and animal levels. Metabolomics was performed to analyze differential metabolites and metabolic pathways. Furthermore, we examined the regulatory mechanisms of BPGM by HIF-1α in NAFLD. Results indicated that high expression of BPGM in NAFLD samples was correlated with NAFLD progression. Moreover, Severe group had higher BPGM expression than Mild group. FFA treatment induced time-dependent steatosis and BPGM upregulation in HepG2 cells and liver organoids, whereas BPGM knockdown attenuated lipid accumulation, cellular injury, and oxidative stress. At the animal level, knockdown of BPGM reversed high-fat diet (HFD) induced lipid accumulation and liver tissue injury. Metabolomics studies showed significant changes of metabolic pathways including glycolysis/gluconeogenesis and pyruvate metabolism. Verification experiment showed FFA increased pyruvic acid levels, and knockdown of BPGM decreased pyruvic acid levels. Pyruvic acid further reversed the changes in NAFLD progression caused by BPGM knockdown at the cellular and organoid levels. Finally, HIF-1α regulated the expression of BPGM in NAFLD. Together, our findings suggest that BPGM contributes to abnormal glucose metabolism and promotes hepatic steatosis, thereby driving NAFLD progression.

Environmental changes and human activities such as deforestation and expansion of agricultural land are increasing tick-borne diseases including Anaplasmosis, Babesiosis, Ehrlichiosis, and Theileriosis. These diseases, which affect animals, can be transmitted to humans through tick bites. Kiambu County's warm, wet climate provides an environment conducive to tick breeding and development. This study investigated the circulation and genetic diversity of Theileria parva and Anaplasma spp. in tick samples collected from Kiambu County, Kenya. Ticks were collected from cattle, goats, and sheep using animal grooming methods and morphologically identified and organized into 129 pools. Total DNA was extracted from tick pools using the sodium dodecyl sulfate extraction method. The 18S rRNA hypervariable region was amplified for T. parva detection, and the 16S rRNA gene was used for Anaplasma spp. detection. A total of 716 ticks were collected, with Rhipicephalus evertsi evertsi (n = 585, 81.7%) being the most abundant species. Molecular analysis indicated the presence of T. parva in n = 8 pools of Rh. e. evertsi. Anaplasma species was detected in three pools of Rh. e. evertsi, one pool of A. variegatum, and one pool of H. truncatum. Phylogenetic analysis revealed that eight T. parva samples clustered closely with isolates from Uganda and Mexico, suggesting potential historical or ecological links between regional isolates and international strains, although direct transmission cannot be confirmed. For Anaplasma spp., phylogenetic analysis identified Anaplasma ovis and Anaplasma bovis in ticks collected from cattle and sheep, including Rh. e. evertsi, A. Variegatum, and H. truncatum, with single nucleotide polymorphisms (SNPs) identified within the Anaplasma sequences. The findings emphasize the importance of continued molecular surveillance of tick-borne pathogens, characterization, and the development of targeted tick control measures to mitigate the impact of tick-borne diseases in livestock.

Alzheimer's disease (AD) research has primarily focused on amyloid beta (Aβ) and tau protein; however, drug development targeting these two proteins has been disappointing. Therefore, there is an urgent need to explore the novel pathogenic mechanisms underlying AD. Recently, we found that expression of the K670N/M671L-mutated amyloid precursor protein (APP) in 293T cells significantly reduced membrane ferroportin (FPN) levels. Furthermore, 2-month-old APP/PS1 mice exhibited a marked decrease in membrane FPN levels, while total FPN expression and Aβ levels remained unchanged. Further studies revealed that features of ferroptosis were present in the brains of 2-month-old APP/PS1 mice, and that treatment with ferroptosis inhibitors or iron chelation significantly alleviated early pathological changes and cognitive impairment in these animals. In addition, supplementation with an APP-FPN binding peptide during the early phase ameliorated AD-related pathologies, including Aβ deposition, neuroinflammation, oxidative stress, and synapse-associated protein deficits, in APP/PS1 mice. Collectively, our findings suggest that APP mutations may contribute to early brain pathological changes and subsequent memory impairment in AD by downregulating membrane trafficking of FPN and inducing ferroptosis, thereby providing new molecular targets for drug development.

Metabolic inflammation, triggered by obesity is a core pathological link in complications such as type 2 diabetes, cardiovascular diseases, and non-alcoholic fatty liver disease. This review explains the central hub role of microRNAs in obesity-related chronic low-grade inflammation, achieved through their precise regulation of macrophage polarisation, inflammatory signalling pathways, and adipokine secretion. Importantly, this relationship is bidirectional-while miRNAs regulate inflammatory cascades, the inflammatory environment itself can alter miRNA expression, forming complex feedback loops. Circulating miRNAs, due to their stability (conferred by encapsulation in exosomes or binding to proteins), tissue specificity, and strong correlation with pathological processes, show great potential as promising non-invasive biomarkers for metabolic inflammation, useful for assessing its activity and complication risk. Furthermore, miRNA-based intervention strategies have demonstrated significant metabolic improvements in animal models. However, their clinical translation still faces challenges such as insufficient delivery targeting, off-target effects, and pharmacokinetic defects. This article aims to summarise the regulatory network of miRNAs in metabolic inflammation and discuss in depth their potential and the bottlenecks to be solved for moving from basic research to clinical application, providing new theoretical basis and strategic directions for the diagnosis and targeted therapy of obesity-related metabolic diseases.

Sturge-Weber Syndrome (SWS) is a rare congenital disorder presenting with a vascular malformation in the upper face and brain, causing impaired blood-brain barrier function and perfusion, increased calcium signaling, inflammation, and seizures. All these neuropathologic processes result in injury to the brain. The somatic GNAQ R183Q variant, which accounts for the majority of SWS cases, increases signaling through MAPK, PI3K, mTOR, and inflammatory pathways, primarily in endothelial cells. The discovery of this variant enabled the creation of transgenic and genetic animal and cell culture models. Generating in vitro models has been challenging due to the mosaic nature of SWS, and attempts to separate unaffected from mutant cells in primary culture have failed, limiting the utility of in vitro work. Ongoing in vitro work seeks to overcome these limitations, shape our understanding of SWS, and lead to translational advances in treatment and prevention by studying the affected molecular pathways and identifying future targets for therapy.

The river buffalo is an economically important livestock species supplying milk and meat. However, a multi-tissue transcriptomic atlas for the key dairy river buffalo breeds, Murrah and Nili-Ravi, has not yet been established, and the lack of stable reference genes has hindered in-depth studies of their biological functions and the molecular mechanisms underlying key economic traits such as lactation. We established a multi-tissue gene expression atlas across 20 tissues and identified 717 housekeeping genes (HKGs), and RPL37A and EEF2 were further shown to be stable candidate reference genes under the conditions tested. We found 8368 tissue-specific genes (TSGs), predominantly enriched in the reproductive system. Exploratory analysis of mammary tissue (dry-period vs. public lactating samples, confounded by batch effects) revealed mammary-enriched hub genes including LALBA; these findings are preliminary and require validation. Dynamic analysis across lactation stages (early, peak, mid-, late) identified candidate genes including SEC14L2 and ACSM3. Phenotypic data showed strong negative correlations between milk yield and protein/fat content, and a positive correlation with lactose content. However, causal or regulatory roles were not inferred due to lack of paired individual-level data. Cross-dataset comparisons are descriptive only, and are not key conclusions. In summary, this study lays the foundation for advancing research in lactation trait genetics and functional genomics in river buffalo, with novel reference genes and lactation stage-specific transcriptional dynamics as its main contributions.

Galectins are a functionally diverse family of β-galactosyl-binding lectins that are ubiquitously present in animal species, with key roles in development and immune regulation. Recently, galectins have been found to recognize microbial glycosylated moieties, but the detailed mechanisms of their innate immune functions in mucosal epithelia have remained elusive. The zebrafish (Danio rerio) represents an ideal genetically tractable model to address these questions, as the skin, gills, and gut display mucosal surfaces exposed to the environment. In this study, we investigated the range of endogenous and microbial glycans that are recognized by zebrafish galectin Drgal1 present in epidermal mucus, which would be consistent with defense functions against a bacterial challenge. Results revealed that zebrafish galectin isoform Drgal1-L2 can recognize selected bacterial glycans, as well as zebrafish mucus glycans and cell-surface receptors for bacterial adhesins such as fibronectin (KD = 1.593 × 10-6 M) and CD147 (KD = 1.115 × 10-6 M). Furthermore, preliminary experiments revealed that Drgal1-L2 may hinder bacterial adhesion to epidermal mucus in about 50% at 2.5 μg/mL. Our results suggest that Drgal1-L2 present in epidermal mucus can prevent access of pathogenic bacteria to the epithelial cell surface by alternate or synergic binding to bacterial glycans and to zebrafish mucus components and epithelial receptors for bacterial adhesins. Thus, the present study provides key information for the testing of the abovementioned hypothesis by implementing gene-silencing approaches targeting both zebrafish Drgal1-L2 and its ligands.

Unmapped sequencing reads in livestock often contain valuable information about pathogens but are typically discarded. We analyzed blood-derived DNA and RNA from chickens and pigs kept under high- and low-biosecurity conditions, focusing on unmapped reads. In chickens, low-biosecurity farms harbored substantially more viral sequences, primarily plant viruses, indicating environmental contamination. In pigs, Mycoplasmoides pneumoniae and several pig-specific viruses were detected. Our bioinformatics pipeline, involving host read removal, assembly, BLAST, and taxonomic filtering, efficiently identified candidate pathogens and contaminants. This approach demonstrates the potential of sequencing-based environmental DNA monitoring to track microbial and viral presence, assess farm biosecurity, and support animal health surveillance.

Linezolid represents a critical last-resort treatment for severe multidrug-resistant (MDR) Gram-positive bacterial infections. Rising linezolid resistance in Enterococcus isolates threatens its efficacy; this study characterized the molecular features and transfer potential of plasmid-encoded linezolid resistance genes optrA and poxtA in a linezolid-resistant Enterococcus asini isolate from chickens. An E. asini strain was isolated during a surveillance program focusing on drug-resistant Gram-positive bacteria in poultry. PCR screened linezolid resistance genes, conjugation and plasmid stability assays evaluated gene transferability and stability, and whole-genome sequencing (WGS) was performed using both the Illumina and Nanopore platforms. We present the first detection of optrA and poxtA genes in E. asini recovered from chicken feces in China. Sequence analysis of the complete genome showed that poxtA and optrA were situated on two distinct plasmids. The poxtA positive plasmid, pHNGXN23C145Ea-1, also carried multiple resistance genes, including tet(S), fexB, erm(B), ant(6)-Ia, aph(3')-III. Furthermore, the poxtA gene was flanked by IS1216E mobile elements. The optrA bearing plasmid, pHNGXN23C145Ea-2, harbours a common genetic array of 'IS1216E fexA-optrA-erm(A)-IS1216E'. Conjugation experiments indicated that neither the poxtA- nor the optrA-bearing plasmid was transferred to recipient strains, which was consistent with sequence analysis showing that both plasmids lacked intact conjugative transfer regions. Stability assays confirmed that poxtA and optrA remained highly stable in the absence of selective pressure. Notably, this discovery was made in a livestock sample, despite the non-use of linezolid in food animals, suggesting that such niches may act as silent reservoirs for resistance genes, which could persist and potentially transfer to clinically relevant MDR pathogens.

This study elucidated several plasma proteins that are causally linked to the risk of diabetic neuropathy (DN), offering novel insights into the protein-mediated DN pathogenesis and potential targets for therapeutic intervention. We employed Mendelian randomization (MR) utilizing genome-wide association study (GWAS) data to evaluate the causal effects of 4,907 proteins on DN. We retrieved a high-throughput sequencing dataset (GSE148061, containing 53 DN patients and 53 healthy donors) from the Gene Expression Omnibus (GEO) database to perform differential gene analysis and functional enrichment analysis, aiming to clarify disease pathogenesis. The MR findings were subsequently validated through Bayesian colocalization analysis and cluster identification. We utilized two machine learning algorithms: Least Absolute Shrinkage and Selection Operator (LASSO) and Random Forest (RF). Further, Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) were conducted on these key genes to uncover the underlying molecular mechanisms influencing DN. Finally, we constructed a DN mouse model to validate the diagnostic potential of these identified genes. We identified seven plasma proteins significantly associated with DN. By integrating Bayesian colocalization, various datasets, and two machine learning methods, we determined that the HSPB1, KRT14, and SFN genes are the most robust diagnostic biomarkers and key mediators. These genes were primarily enriched in the Wnt Signaling Pathway, Regulation of ERK1 and Cascade, Negative Regulation of MAPK Cascade, and Alditol Phosphate Metabolic Process. The expression changes of HSPB1, KRT14, and SFN were further validated using animal models. This study systematically identified HSPB1, KRT14, and SFN as potential biomarkers for patients with DN.

Osteoporosis is a metabolic bone disease characterized by reduced bone mass and deterioration of bone microarchitecture, in which impaired osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) represents a central pathological mechanism. In recent years, ferroptosis, a newly recognized form of regulated cell death, has been demonstrated to play an important role in the initiation and progression of osteoporosis. Mitochondrial dysfunction can exacerbate oxidative stress and disrupt iron metabolism, thereby triggering ferroptosis in BMSCs and ultimately inhibiting osteogenic differentiation. The present study aimed to identify and validate key genes associated with mitochondrial homeostasis and osteoporosis, with a particular focus on the role of glial cell line-derived neurotrophic factor (GDNF) in regulating mitochondrial function, suppressing ferroptosis, and promoting osteogenic differentiation of BMSCs. Gene expression data from normal human bone tissues and osteoporotic bone tissues were obtained from public transcriptomic datasets in the Gene Expression Omnibus (GEO) database. Through differential expression analysis, GDNF was identified as a candidate gene. In vitro experiments demonstrated that GDNF markedly improved mitochondrial membrane potential, reduced intracellular reactive oxygen species (ROS) levels, and restored GPX4 expression, thereby promoting osteogenic differentiation of BMSCs. Furthermore, animal experiments confirmed that GDNF intervention effectively increased bone mineral density and improved trabecular microarchitecture in ovariectomized (OVX) mice. In conclusion, this study identified GDNF may suppress ferroptosis by maintaining mitochondrial homeostasis in BMSCs, thereby enhancing osteogenic differentiation and alleviating osteoporosis, providing a potential theoretical basis for molecular targeted therapy in osteoporosis.

Generalized epilepsy with febrile seizures plus (GEFS+) is an inherited epileptic disorder predominantly linked to autosomal-dominant, loss-of-function mutations in the sodium voltage-gated channel α subunit 1 (SCN1A) gene, which encodes the α subunit of the neuronal voltage-gated sodium ion channel type 1 (NaV1.1). Reduced NaV1.1 function in γ-aminobutyric acid (GABA)-ergic interneurons impairs inhibitory signaling and leads to neuronal hyperexcitability. Clinically, GEFS+ is characterized by a spectrum of seizure types, often beginning with febrile seizures in early childhood and progressing to generalized tonic-clonic seizures later in life. Here, we used prime editing to correct the pathogenic SCN1A-K1270T mutation in the Scn1aKT/+ mouse model of GEFS+. Adeno-associated viral (AAV) vectors were used to deliver an intein-split prime editor under the control of a neuron-specific promoter into the cerebral ventricles of neonatal mice. This enabled efficient in vivo editing, achieving 34.7 ± 14.5% correction of the mutant allele in cortical bulk DNA, 81.2 ± 5.9% correction of mRNA, and improved multiple disease-relevant phenotypes. Survival increased from 80% in control-treated animals to 100% in treated mice, cortical inhibitory neuron transmission was improved (frequencies of inhibitory postsynaptic currents were increased from 0.32 to 1.32 hertz), and the frequency of induced febrile seizures decreased from 78.6% to 13.3%, approaching the frequency seen in wild-type mice (8%). These findings suggest the therapeutic potential of prime editing for the treatment of patients with SCN1A-associated GEFS+.

Cancer therapy is increasingly shaped by the need for agents that are both mechanistically precise and clinically tolerable. Sulforaphane (SFN), a dietary isothiocyanate enriched in cabbage-family vegetables such as cauliflower and Brussels sprouts, has emerged as a pleiotropic modulator of tumor biology. This review synthesizes current evidence that SFN regulates diverse cancer-relevant processes, including redox homeostasis, cell-cycle progression, apoptosis, autophagy and epigenetic remodeling, largely through coordinated effects on transcriptional (for example, Nrf2, MAPK, NF-κB and AP-1), post-transcriptional (microRNAs and messenger RNAs) and epigenetic (DNA methyltransferases and histone deacetylases) networks. We then examine how functional nucleic acids, including aptamers, small interfering RNAs, microRNAs and tetrahedral DNA nanostructures, can be engineered to guide SFN to tumor cells, amplify pathway-specific effects and overcome resistance. Particular emphasis is placed on nanotechnology-enabled delivery platforms that enhance SFN stability, bioavailability and tumor selectivity. Finally, we outline key challenges, such as context-dependent Nrf2 activity, inter-individual variability in metabolism and incomplete clinical validation, and propose priorities for translating SFN-based functional nucleic acid systems into rational, combination-ready strategies for precision oncology.

The current study aimed to determine the current status, genetic diversity, and molecular characterization of Newcastle disease viruses (NDV) isolated from chicken in Egypt during the period between 2019 and 2024. Out of 739 samples examined, 101 (14%) tested positive for NDV by real-time reverse transcription polymerase chain reaction (RT-qPCR). Positive cases were confirmed in 17 out of the 24 governorates studied which accounts for 71% of the locations where samples were collected. The majority of these cases (82 out of 664) were from chicken farms with 18 cases from other poultry species. Forty seven out of the 101 NDV isolates from chicken were selected for partial F gene sequence analysis. Based on F gene partial sequence analysis, 44 strains from chicken were classified as NDV genotype VII which is prevalent in poultry species in Egypt, and three isolates were categorized as Class II closely related to LaSota vaccine strains. However, the complete genomic sequencing of F gene revealed that all five isolates were associated with sub genotype VII.1.1. The avirulent strains of the viruses displayed the 112GRQGRL117 motif, while the virulent strains revealed the 112RRQKRF117 motif. Mutations were also found in the F gene which encompassed a region of the effect, such as the cleavage site, the cystoplasmic domains, and the HR domains. Investigation of the glycosylation site revealed that six N-linked glycosylation motifs were located in the F gene at residues 85, 191, 366, 447, 471, and 541 and in the HR domains 191 and 471. This study concludes the requirement of strict biosecurity measures combined with updated vaccination strategies to control NDV in poultry.

Alzheimer's disease (AD) is increasingly recognized as a multisystem neurodegenerative disorder in which sensory dysfunction accompanies cognitive decline. As an accessible extension of the central nervous system, the retina provides a valuable window for investigating early neurodegenerative processes; however, the cellular mechanisms underlying AD-associated retinal pathology remain incompletely understood. Here, using the APP/PS1 mouse model, we systematically examined structural, functional, and glial alterations in the retina across disease stages. Despite robust age-dependent amyloid plaque accumulation in visual-related brain regions, no plaque-like β-amyloid (Aβ) deposits were detected in the retina even at advanced ages. Nevertheless, young APP/PS1 mice exhibited early thinning of inner retinal layers, impaired retinal electrophysiological responses, and reduced excitatory synaptic inputs to retinal ganglion cells (RGCs), preceding overt neuronal loss. These neuronal changes were accompanied by pronounced Müller glial activation, characterized by upregulation of gliosis markers and extensive morphological remodeling. Functional analyses further revealed dynamic alterations in glial homeostasis, including early elevation followed by age-dependent decline of glutamine synthetase activity, together with increased expression and disrupted perivascular polarity of aquaporin-4. Consistently, transcriptomic profiling of young AD retinas identified coordinated dysregulation of genes involved in amino acid metabolism, transport, and oxidative stress responses. Together, our findings identify Müller glial remodeling as an early feature of AD-associated retinal pathology that coincides with synaptic vulnerability of RGCs and occurs independently of local Aβ plaque deposition, highlighting retinal glia as potential early indicators and modulators of neurodegeneration.