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Ulcerative colitis (UC) is subtype of inflammatory bowel disease that is frequently comorbid with anxiety disorders. However, effective dual-targeting therapies are still lacking. Hyperoside (HYP), a natural flavonoid, exhibits anti-inflammatory and neuroprotective properties, yet its potential therapeutic effects on UC and associated anxiety, as well as the underlying mechanisms, remain largely unexplored. A murine model of DSS-induced colitis was established and treated with HYP. Disease activity was assessed through body weight, colon length, and histopathology. Anxiety-like behaviors were evaluated using open field and elevated plus maze tests. Neuroinflammation was examined through immunohistochemistry of BDNF expression and microglial activation. Gut microbiota composition was profiled by metagenomic sequencing, and metabolomic profiling was conducted using the Q300 Kit. Network pharmacology and molecular docking were employed to predict signaling pathways, which were further validated by Western blotting. Additionally, antibiotic depletion experiments were conducted to determine microbiota dependency. HYP administration significantly ameliorated DSS-induced colitis, as evidenced by attenuated weight loss, restored colon length, and improved histopathology. It suppressed pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and restored intestinal barrier integrity by upregulating Mucin-2 and ZO-1. Furthermore, HYP also alleviated anxiety-like behaviors and mitigated neuroinflammation by increasing BDNF levels and suppressing microglial activation. HYP treatment also restored gut microbial homeostasis, enriching beneficial bacteria such as Our findings demonstrate that HYP effectively alleviates DSS-induced colitis and comorbid anxiety-like behaviors. Its efficacy is dependent on the gut microbiota and is associated with the restoration of microbial homeostasis, enhancement of arginine metabolism, and modulation of the MAPK/PI3K-Akt/NF-κB signaling pathways. HYP represents a promising microbiota-targeting therapeutic candidate for UC and its neuropsychiatric comorbidities. Show less

FGFRs genetic alterations such as mutations, amplifications, and chromosomal translocations are prevalent in cancers, leading to the initiation and progression of tumors by enhancing FGFR signaling. The substantial problems arising from the lack of decisive clinical evidence have resulted in the cessation of some inhibitor applications, and identifying effective small molecule inhibitors that selectively target FGFRs can advance the therapy of cancers driven by FGFRs abnormalities. The three-dimensional structure of the FGFR1/2/3/4 protein and the amino acid positions within the tyrosine kinase domain were downloaded from the PDB database, and small molecule data were extracted from the ZINC15 database. Then, we used molecular docking and dynamics simulations to assess compounds interacting with FGFR proteins, and screening potential small molecules targeting FGFR. Finally, we evaluated its effects by two CRC cell line HCT116 and NCI-H716. In the study, by docking with 2.8 million small molecules, we identified three promising FGFR small molecule inhibitors ranked in the top average absolute difference in free energy. By evaluating the binding stability of the docking pose of the three compounds, we found that ZINC000101867325 could form the stable binding interactions with FGFR1/2/3. And, ZINC000101867325 inhibited the activity of FGFR signaling, and resulted in cell apoptosis and decrease in cell proliferation and migration in colorectal cancer cell lines. In addition, ZINC000101867325 is also predicted to target FGFR2 mutations in colorectal cancer patients. We predicted three small molecules targeting FGFRs, and ZINC000101867325 shows superior chemical bond types and stability with FGFR1/2/3, and inhibits FGFR signaling in CRC cell lines. This study provides novel FGFRs inhibitors, which enrich treatment strategies for cancers. Show less

Alzheimer's disease (AD) is the most prevalent form of dementia, accounting for more than two-thirds of cases in older adults. AD is associated with neuropsychiatric symptoms such as depression, anxiety, and sleep disturbances. The coexistence of AD with depression, in particular, poses serious challenges and often results in suboptimal outcomes with conventional therapies. The present study therefore aimed to investigate the therapeutic potential of escitalopram (ESC; SSRI) in combination with galantamine (GAL; AChE inhibitor) on key pathological pathways, including the neurotrophic system, hypothalamic-pituitary-adrenal (HPA) axis, kynurenine pathway, inflammation, and oxidative stress, in an animal model of AD comorbid with depression. Swiss albino mice were subjected to chronic mild stress (CMS) for 21 days and received intrahippocampal administration of amyloid-β peptide to mimic AD-depression comorbidity. Subsequently, ESC (10 mg/kg) combined with GAL (5 mg/kg) was administered orally for 20 days alongside the CMS protocol, followed by behavioral, biochemical, and histopathological assessments. The combined GAL + ESC treatment significantly alleviated depressive symptoms and improved working and spatial memory in CMS and amyloid-β-exposed mice. Furthermore, the therapy normalized hippocampal levels of BDNF, proinflammatory cytokines (IL-6, TNF-α), kynurenine metabolites (3-HK, QUIN), and oxidative stress markers toward those observed in the sham group. Histopathological analysis further confirmed the preservation of hippocampal integrity with combined therapy. Overall, the findings highlight the potential of ESC as an adjunct to GAL in ameliorating depressive symptoms and cognitive deficits, underscoring its promise for further clinical evaluation in the management of AD comorbid with depression. Show less

Pain is one of the leading causes of disability worldwide. Despite the various pharmacological treatments available, patients with chronic pain often remain with significant disabilities and unsatisfactory pain control. Cannabis and cannabinoids are sometimes used in the treatment of chronic pain as they have been shown to be useful in a subset of patients. Some of the adverse effects associated with cannabis use, such as cannabis use disorder (CUD) and cannabis-induced psychosis, have been associated with several genetic variants. Despite this, the paucity of the data or the contradictory results for reported variants limits our ability to use them as genetic markers to personalize cannabis treatment tailored to patients’ genetic background. The aim of this genetic association study was to investigate the link between previously reported genes and cannabinoid response in terms of pain response, CUD and risk of psychotic adverse events in patients with chronic pain. Phone or in person interviews were conducted to document participants’ characteristics, cannabis use and effects, concurrent pharmacotherapy and comorbid conditions. Screening for CUD was performed using the Cannabis Use Disorders Identification Test – Revised. Blood or saliva samples were collected for the genotyping of 18 variants in 11 genes ( One hundred participants were recruited, with blood or saliva samples collected from 77 of them. Two single-nucleotide polymorphisms (SNP) in cannabinoid receptor 1 ( These results suggest alternative allele carriers of rs1049353 and rs2023239 could be at an increased risk of psychotic adverse events related to cannabis use, although additional investigation is required to replicate and confirm these findings. The online version contains supplementary material available at 10.1186/s42238-026-00408-w. Show less

Gibberellins have been reported to play both positive and negative roles in arbuscular mycorrhizal (AM) symbioses. Despite extensive characterisation of the role of DELLAs in AM colonisation, studies of gibberellin function have largely been restricted to chemical interventions. Few studies have examined how disruption to gibberellin biosynthesis affects AM symbioses. To explore this further, we obtained Show less

The apolipoprotein E (APOE) ε4 allele is a risk factor for late-onset Alzheimer's disease; however, risk varies by sex and lifestyle. Regular physical activity is known to mitigate cognitive decline; whether the degree of benefit differs by APOE genotype, sex, and race remains unknown. Analyses utilized data from 2,985 participants in the Health, Aging, and Body Composition (HABC) cohort, comprising community-dwelling black and white older adults followed for 10 years. Cognitive performance was assessed multiple times across the 10 years using the Digit Symbol Substitution Test (DSST) for executive functions and processing speed and the Modified Mini-Mental State Examination (3MS) for global cognition. APOE genotypes were categorized into ε2, ε3, and ε4 groups. Annual self-reported walking time was used to quantify physical activity. Linear mixed models and latent growth curve modeling examined the interactions between APOE genotype, sex, and walking on cognitive trajectories with adjustments for race, study location, health score, age, education attained, and body mass index. APOE ε4 carriers demonstrated steeper declines in both DSST and 3MS scores compared to ε3 carriers, irrespective of sex (all β<-0.13, all p < 0.004). APOE ε2 was protective longitudinally for 3MS in females only (β = 0.15, p < 0.002). Walking showed the strongest protective effect in APOE ε4 carriers for females and males in the rate of change of DSST and 3MS scores (all β > 0.27, all p < 0.044). These findings underscore the importance of public messaging about the benefits of regular physical activity for retaining cognitive function especially for persons genetically at heightened risk. Show less

Object recognition memory (ORM) plays a key role in identifying familiar items and encoding episodic information. ORM consolidation depends on β-adrenergic receptor (βAR) signaling and is associated with increased BDNF expression in the dorsal hippocampus. Although hippocampal activation of cannabinoid type-1 receptors (CB1Rs) is known to impair ORM consolidation, the mechanisms underlying this effect remain unclear. In this study, we used the novel object recognition task to examine the interaction between CB1Rs and βARs during ORM consolidation in adult male Wistar rats. Intra-dorsal CA1 infusion of the CB1R agonist ACEA, the βAR antagonist propranolol, or the PKA inhibitor myristoylated PKI Show less

The neurotrophic factor (NTF) family has recently expanded its role beyond neurological conditions, but its involvement in acute inflammatory lung diseases remains largely unclear. Using well-established acute lung injury (ALI) and sepsis models, we demonstrate that brain-derived neurotrophic factor (BDNF), a key NTF, is impaired in pulmonary epithelial cells and negatively correlates with the inflammatory response. Raising the BDNF level alleviates inflammatory lung injury, but these effects are absent in macrophage-deleted mice. Both in vivo and in vitro results show BDNF inhibits macrophage inflammation, and further proteomics analysis identifies macrophage TLR4 as a receptor that BDNF antagonizes via direct binding. The BDNF fragment (aa 104-115) is critical for BDNF-TLR4 interaction, and the corresponding synthetic BDNF-derived dodecapeptide (BDP-12) retains TLR4-antagonistic and anti-inflammatory effects both in vitro and in vivo, without pro-proliferative side effects. In conclusion, our findings reveal that epithelial-derived BDNF prevents macrophage inflammation by directly targeting TLR4 and highlights BDP-12 as a potential therapeutic agent for acute inflammatory diseases. Show less

Osteoporosis frequently affects older women and is strongly linked to their daily routines, which include both sedentary behavior (SEB) and physical activities (PA) of different intensities. This study investigates the dose-response relationship of different SEB and PA patterns among community-dwelling older women and assesses the potential impact of time reallocation on osteoporosis risk through an isotemporal substitution analysis. In this study, 1,106 older women aged between 60 and 70 years in Tianjin participated. Their moderate to vigorous physical activity (MVPA), light physical activity (LPA), and SEB were objectively assessed using an accelerometer. The connection between MVPA, LPA, SEB, and osteoporosis was assessed using binary logistic regression models and isotemporal substitution models. The osteoporosis group and non-osteoporosis group comprised 461 and 645 subjects respectively, accounting for 41.68 and 58.32% of the total cohort. The osteoporosis group had significantly higher daily SEB compared to the non-osteoporosis group ( PA and SEB in older women exhibit a significant dose-response relationship with osteoporosis. Avoiding prolonged sitting and increasing PA duration both offer protective effects against osteoporosis in older women, with achieving a certain level of MVPA being the most effective protective measure. Show less

The maternal perinatal environment shapes brain development and long-term neurodevelopmental trajectories. Probiotic supplementation during this period has emerged as a promising strategy to support healthy neurodevelopmental outcomes through modulation of immune and synaptic plasticity pathways. However, the persistence and specificity of molecular effects in the offspring brain, particularly with respect to sex and brain region, remain poorly understood. We conducted two independent mouse experiments using different probiotic strains and exposure windows to evaluate the long-term transcriptional effects of maternal probiotic supplementation. Time-mated C57BL/6JRj dams received a multi-species probiotic (Ecologic® Panda) from gestational day (GD) 6 until birth, whereas BALB/cJRj dams received Multi-species supplementation induced broad and persistent transcriptional changes in hippocampus and hypothalamus, with generally larger effects in males. Altered transcripts included markers of synaptic plasticity ( These findings highlight that short, targeted maternal probiotic supplementation during the perinatal period is associated with persistent molecular signatures in the adult offspring brain across genetic backgrounds, converging on neuroimmune-related pathways. Show less

Hypertrophic scar (HS) is a fibroproliferative disorder characterized by fibroblast hyperactivation and aberrant extracellular matrix deposition. This study identifies macrophage-derived lactate as a key mediator of fibroblast phenotypic remodeling via monocarboxylate transporter 1 (MCT1)-mediated histone H3 lysine 23 lactylation (H3K23la) in HS. Elevated lactate levels and MCT1 expression were observed in HS tissues, with macrophages in stiff mechanical microenvironments identified as the primary lactate source. Lactate influx through MCT1 upregulated H3K23la, thereby promoting transcriptional activation of profibrotic genes HEY2 and COL11A1. Mechanistically, HEY2 activated YAP1/SMAD2 signaling, while COL11A1 stabilized MCT1 to enhance lactate transport, forming a positive loop that amplified fibrosis. Fibroblast-specific Mct1 deletion or pharmacological inhibition of Mct1 in male mice reduced collagen deposition, accelerated wound healing, and attenuated scar formation. Our findings redefine the macrophage-fibroblast crosstalk in HS and establish the MCT1-H3K23la-HEY2/COL11A1 axis, particularly its self-reinforcing loop, as a novel therapeutic target. Show less

Prostate cancer (PCa) is the most common male cancer and the second leading cause of cancer death in men. Androgen deprivation therapy (ADT) has been widely used as the first-line treatment for PCa. However, most PCa will progress to castration-resistant PCa (CRPC) that resists ADT 1 to 3 years after the treatment. Steroidogenesis from cholesterol is one of the mechanisms leading to ADT resistance. In PCa cells, low-density lipoprotein (LDL) mediated uptake is the major venue to acquire cholesterol. However, the mechanism of regulating this process is not fully understood. Fibroblast growth factor receptor 1 (FGFR1) is a receptor tyrosine kinase (RTK) that is ectopically expressed in PCa cells and promotes PCa progression by activating downstream signaling pathways. To comprehensively determine the roles of FGFR1 in PCa, we generated FGFR1-null DU145 cells and compared the transcriptomes of FGFR1-null and wild-type cells. We found that ablation of FGFR1 reduced the expression of genes promoting LDL uptake and de novo synthesis of cholesterol, thereby reducing the overall cholesterol pool in PCa cells. Detailed mechanistic studies further revealed that FGFR1 boosted the activation of sterol regulatory element-binding protein 2 (SREBP2) through ERK-dependent phosphorylation and cleavage, which, in turn, increased the expression of low-density lipoprotein receptor (LDLR) and enzymes involved in de novo cholesterol synthesis. Furthermore, in silico analyses demonstrated that high expression of FGFR1 was associated with high LDLR expression and clinicopathological features in PCa. Collectively, our data unveiled a previously unrecognized therapeutic avenue for CRPC by targeting FGFR1-driven cholesterol uptake and de novo synthesis. Show less

Fibroblast growth factor receptor 1 (FGFR1) is recurrently mutated at p.N546 in neuroblastoma. We examined whether mutant FGFR1 is an oncogenic driver, a predictive biomarker, and an actionable vulnerability in this malignancy. FGFR1 mutations at p.N546 were associated with high-risk disease and rapid tumor progression, resulting in dismal outcome for these patients. Ectopic expression of FGFR1N546K induced constitutive downstream signaling and IL-3-independent growth in Ba/F3 cells, indicating oncogene-addicted proliferation. In FGFR1N546K;MYCN transgenic mice, neuroblastoma developed within the first days of life, with fatal outcome within 3 weeks, reflecting the devastating clinical phenotypes of patients with FGFR1-mutant, high-risk neuroblastoma. Treatment with FGFR inhibitors impaired proliferation and pathway activation in FGFR1N546K-expressing Ba/F3 and patient-derived FGFR1N546K-mutant neuroblastoma cells and inhibited tumor growth in FGFR1N546K;MYCN transgenic mice and in a chemotherapy-resistant, patient-derived xenograft mouse model. In addition, partial regression of FGFR1N546K-mutant tumor lesions occurred upon treatment with the FGFR inhibitor futibatinib and low-intensity chemotherapy in a patient with refractory neuroblastoma. Together, our data demonstrate that FGFR1N546K is a strong oncogenic driver in neuroblastoma associated with failure of current standard chemotherapy and suggest potential clinical benefit of FGFR-directed therapies in patients with high-risk mutant FGFR1. Show less

Cereal vinegar sediment (CVS), a byproduct of traditional vinegar fermentation, has been regarded as a health-promoting product. However, its role in genetically induced hyperlipidemia remains unclear. This study systematically evaluated the effects of Dade-CVS (DD-CVS) and Hengshun-CVS (HS-CVS) on apolipoprotein-E-deficient ( Show less

Flavonoids are a diverse group of natural polyphenolic compounds, recognized for their ability to modulate cellular pathways and mitigate the pathological processes of many neurodegenerative diseases. This study investigates the neurotrophic potential of a polyphenolic-rich lemon peel extract (Lpe) in a Zebrafish larvae spinal cord injury (SCI) model. To evaluate its potential effects, embryos were divided into six experimental groups: a baseline control group in which larvae were neither subjected to spinal cord injury nor treated (Ctrl Group); a group with larvae subjected to spinal cord injury at 3 dpf without treatment (SCI Group); a group treated continuously with Lpe (25 µg/mL) from 0 to 5 dpf without injury (Continuous Group); a group treated continuously with Lpe and injured at 3 dpf (Continuous SCI Group); a group treated with Lpe starting at 3 dpf without injury (Curative Group); and finally, a group injured at 3 dpf and treated simultaneously with Lpe (Curative SCI Group). Lpe treatment significantly downregulated proinflammatory cytokines ( Show less

Eye drops derived from human blood components (Eye Drops of Human Origin-EDHO) have proven effective in reducing ocular pain associated with severe keratopathies. Among these, Cord Blood Serum (CBS) is particularly promising for its high content of growth and neurotrophic factors. This study evaluated the ability of CBS to modulate inflammatory and nociceptive activation in the human conjunctival epithelial cell (HCEC) line exposed to hyperosmotic stress. CBS batches were characterized for brain-derived neurotrophic factor (BDNF) content and classified as CBS Show less

Although aneuploidy is generally detrimental to the survival and growth of normal cells, it can be beneficial under certain stress conditions, such as those caused by harmful mutations. In Saccharomyces cerevisiae, we find that duplication of chromosome III accelerates cell proliferation in the orc5-1 mutant. Enhanced proliferation is also observed when a fragment from a different chromosome is introduced, demonstrating that the benefit is not simply due to extra copies of specific genes. A comparable growth-enhancing effect of an extra chromosome is observed for mutations affecting other proteins involved in DNA replication licensing. The suppression of orc5-1 growth defect is also observed in the absence of the G1 cyclin Cln3, which lengthens the G1 phase, while overexpressing CLN3, which shortens G1, has the opposite effect. Additionally, Cln3 loss mirrors the effect of an extra chromosome for other mutations. These findings indicate that the severity of mutations impacting origin licensing hinges on the length of the G1 phase. Thus, we propose that the fitness-enhancing effect of an extra chromosome in DNA replication licensing mutants largely stems from its ability to extend G1, compensating for inefficient origin licensing. Show less

Post-stroke seizures are a common and debilitating complication with limited therapeutic options, underscoring the need to identify novel molecular targets. Disruption of chloride homeostasis via impaired potassium chloride cotransporter 2 (KCC2) activity is a key driver of neuronal hyperexcitability. While microglia are a predominant source of brain-derived neurotrophic factor (BDNF) in the acute phase after brain injury, the role of microglial BDNF and its signaling in KCC2 dysregulation and early post-stroke seizure susceptibility remain poorly defined. Using a middle cerebral artery occlusion-reperfusion (MCAO-R) mouse model and oxygen-glucose deprivation/reoxygenation (OGD/R) in hippocampal neurons, we assessed KCC2 function, neuronal excitability, and seizure susceptibility. Pharmacological tools, including the microglial inhibitor minocycline, the TrkB antagonist K252a, the loop diuretic furosemide (FUR), repurposed here as a KCC2-stabilizing agent, and the KCC2 activator CLP290, were employed. Techniques included immunofluorescence, Western blotting, patch-clamp electrophysiology, electroencephalography (EEG), and behavioral seizure assessment. MCAO-R and OGD/R significantly reduced membrane KCC2 expression, leading to a depolarizing shift in the GABA equilibrium potentials (E Our findings identify microglia-derived BDNF/TrkB signaling as a critical upstream pathway mediating KCC2 dysfunction in early post-stroke seizure. Targeting this axis by inhibiting microglial activation, blocking TrkB, or directly enhancing KCC2 function with activators like CLP290 represents a promising therapeutic strategy for stroke-related epilepsy. Show less

To identify distinct latent frailty profiles using latent profile analysis (LPA) in patients undergoing radiotherapy for head and neck cancer (HNC) and to examine the factors associated with profile membership. A cross-sectional study. This research used data acquired from a major tertiary referral hospital in China. This study recruited 391 HNC patients receiving radiotherapy. Validated instruments included a demographic questionnaire, Charlson Comorbidity Index (CCI), Pittsburgh Sleep Quality Index, FRAIL Scale, Hospital Anxiety and Depression Scale and Perceived Social Support Scale. Profile membership associations were assessed using χ The frailty status of patients can be divided into three different categories: (1) robust group (23.0%), (2) prefrail group (49.6%) and (3) frail group (27.4%). Frailty demonstrated independent associations with nine clinical parameters in adjusted regression models: radiotherapy session frequency, social support, age, CCI score, educational attainment, metastasis, nutritional risk, radiation-induced injuries and serum albumin levels (p<0.05). The distinct frailty profiles identified by LPA can inform the future development of targeted care protocols for specific subgroups (eg, the frail group), with a focus on key predictors such as age and nutritional risk. Show less

Fragile X Syndrome (FXS) is the most common inherited intellectual disability and a leading monogenic cause of autism spectrum disorder (ASD). As a synaptic disorder, FXS involves the loss of Fragile X messenger ribonucleoprotein 1 (FMRP), leading to abnormal dendrite development and immature dendritic spines. Serotonergic signaling, essential for neuronal development and circuit remodeling, has been implicated in ASD and related conditions, including FXS, raising the possibility that serotonergic modulation could ameliorate neurodevelopmental impairments. This study investigated the therapeutic potential of psilocybin, a serotonergic compound, in the validated Fmr1- Show less

This study explored the molecular mechanisms by which T7 peptide-modified liposomal irisin (T7@Lipo@Irisin) alleviates perioperative neurocognitive disorders (PND) via regulation of the AMPK/PGC-1α metabolic pathway. T7@Lipo@Irisin nanoparticles were prepared by thin-film hydration and ultrasonic dispersion and showed favorable physicochemical performance, with an encapsulation efficiency of approximately 85%. Serum analysis of healthy donors (n = 10) and PND patients (n = 6) showed higher IL-6 and TNF-α and lower brain-derived neurotrophic factor (BDNF) in PND. In vitro, T7@Lipo@Irisin restored mitochondrial membrane potential, reduced reactive oxygen species (ROS) accumulation, enhanced Neuro-2a hippocampal neuron viability, and activated the AMPK/PGC-1α axis under oxidative stress. In a PND mouse model, it improved Garcia neurological scores, preserved neuronal morphology, and decreased apoptosis. Multi-omic integration of scATAC-seq/scRNA-seq and TMT-based proteomics demonstrated enhanced neuro-glial crosstalk, epigenetic activation of metabolic/antioxidant genes (e.g., Sirt1, Nfe2l2), and upregulated pathways (mitochondrial function, NAD-dependent metabolism, synaptic homeostasis). Proteomics confirmed upregulation of SIRT1, NDUFS2, and BDNF, forming a network linked to energy metabolism and neural repair. Collectively, T7@Lipo@Irisin mitigates PND by activating AMPK/PGC-1α to enhance mitochondrial function and stabilize the neuro-microenvironment. Show less

Prosaposin (PSAP) is a highly conserved glycoprotein in vertebrates. It is known to be transported into lysosomes and facilitates lysosomal hydrolysis. In addition, PSAP is secreted in various body fluids, including serum. Extracellular PSAP is known to function as a trophic factor for neurons, and recent studies have revealed that PSAP plays a pivotal role in dopaminergic neuron homeostasis. This study examined PSAP expression in the mouse pituitary gland, which is one of the principal sources of circulating hormones innervated by dopaminergic neurons. In situ hybridization showed that PSAP mRNA expression was high in the intermediate lobe (IL), whereas the expression was relatively low and sparse in the anterior (AL) and posterior lobes (PL). Immunohistochemical analyses showed that PSAP immunoreactivity was detected as fine, granular structures in the AL and IL. PSAP immunoreactivity was also observed in glial cells and the Herring bodies of the PL. The IL is innervated by axons from dopaminergic neurons in the periventricular hypothalamic area, and neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), are known to be highly expressed in the IL, where they support these neurons. The results of this study indicate that PSAP plays a pivotal role in the pituitary gland, particularly within the IL. Show less

An original dataset based on a national quota sample in the Czech Republic (n = 490, M = 46.09 y/o, 45.7% women) was used to assess susceptibility to medical (COVID-19) and political (Russian invasion of Ukraine) disinformation. Susceptibility to disinformation was assessed using 30 items addressing contemporary topics. To identify the latent structure underlying these items, an exploratory factor analysis (principal-axis factoring with direct oblimin rotation) was conducted. EFA yielded four correlated factors: one specific to COVID-19 hoaxes/misinformation (F1) and three others pertaining to the political (F2), economic (F3), and moral/ethical (F4) dimensions of the Russian war. In order to identify response patterns, all 30 items from 490 participants were subjected to Latent Profile Analysis (LPA) in which the EFA factors served to interpret the five resulting types: a neutral No Strong Opinion type (48%); two disinformation-resilient types-Rational Pro-Ukrainians (22%) and Anti-Russians (7%); and two disinformation-susceptible types-Pro-Russians (15%) and the Generally Disinformed (9%). The discussion addresses the sizable No Strong Opinion type and the correlation between COVID-19 hoaxes and propaganda disinformation (r = 0.47), which supports the 'monological belief system' concept. The identified types can be further followed prospectively and retrospectively within an ongoing panel study. Show less

Glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) are proteins essential for neuronal survival and implicated in Parkinson's disease (PD) pathophysiology. Although reduced levels of these neurotrophins have been observed in PD, their relationship with disease progression remains unclear. We conducted a systematic review by independently searching four databases using predefined keywords: Parkinson AND (GDNF OR BDNF OR neurotroph) AND (serum OR blood OR cerebrospinal fluid). After screening 2132 records, 35 studies qualified for inclusion. Changes in neurotrophic factors' levels were evaluated in relation to disease severity and duration. Many studies reported a decline in BDNF levels associated with more severe motor symptoms. Some studies noted increased BDNF levels in advanced PD. This pattern may be affected by levodopa treatment, suggesting that elevated BDNF levels in advanced PD could reflect a treatment-related effect rather than disease progression itself. Reduced levels of both GDNF and BDNF were linked to cognitive decline, with BDNF also decreased in PD patients with depression. Serum BDNF levels were associated with motor severity and neuropsychiatric symptoms. BDNF levels in PD may increase with longer disease duration, likely due to levodopa treatment effects. However, lower BDNF levels are seen in cognitive decline and depression, frequent non-motor symptoms of PD. Further research is required to clarify BDNF dynamics and to determine GDNF's role in motor progression and cognitive decline. Show less