BDNF Levels According to Variations in the CACNA1C Gene: Sex-Based Disparity.

The CACNA1C gene encodes the pore-forming alpha-1c subunit of L-type voltage-gated calcium channels. The calcium influx through these channels regulates the transcription of the brain-derived neurotrophic factor (BDNF). Polymorphisms in this gene have been consistently associated with psychiatric disorders, and alterations in BDNF levels are a possible biological mechanism to explain such associations. Here, we sought to investigate the effect of the CACNA1C rs1006737 and rs4765913 polymorphisms and their haplotypes on serum BDNF concentration. We further aim to investigate the regulatory function of these SNPs and the ones linked to them. The study enrolled 641 young adults (362 women and 279 men) in a cross-sectional population-based survey. Linear regression was used to test the effects of polymorphisms and haplotypes on BDNF levels adjusted for potential confounders. Moreover, regulatory putative functional roles were assessed using in silico approach. BDNF levels were not associated with CACNA1C polymorphisms/haplotype in the total sample. When the sample was stratified by sex, checking the effect of polymorphisms on men and women separately, the A-allele of rs4765913 was associated with lower BDNF levels in women compared with the TT genotype (p = 0.010). The AA (rs1006737-rs4765913) haplotype was associated with BDNF levels in opposite directions regarding sex, with lower levels of BDNF in women (p = 0.040) compared to those without this haplotype, while with higher levels in men (p = 0.027). These findings were supported by the presence of regulatory marks only on the male fetal brain. Our results suggest that the BDNF levels regulation may be a potential mechanism underpinning the association between CACNA1C and psychiatric disorders, with a differential role in women and men.

Temperament traits mediate the relationship between CACNA1C polymorphisms and bipolar disorder in cisgender women.

The influence of temperament traits on bipolar disorder (BD) has been investigated. Both temperament traits and BD are partially genetically determined and seem to be influenced by variations in the CACNA1C gene. These variations presented a significant interactive effect with biological sex, although studies that evaluate this relationship are scarce. Here, we assessed the mediation effect of temperament traits on the relationship between two polymorphisms in the CACNA1C gene (rs1006737 and rs4765913) and BD according to sex. This is a cross-sectional study consisting of 878 Caucasian individuals (508 women and 370 men), aged 18-35, enrolled in a population-based study in the city of Pelotas, Southern Brazil. BD diagnosis was evaluated using the clinical interview MINI 5.0, and temperament traits were assessed via the application of the Affective and Emotional Composite Temperament Scale (AFECTS). Mediation models were tested using the modeling tool PROCESS (version 3.3) for SPSS. Bootstrapping-enhanced mediation analyses in women indicated that traits anger (39%) and caution (27%) mediated the association between the rs4765913 SNP and BD, while traits volition (29%), anger (35%), and caution (29%) mediated the association between the AA haplotype (rs1006737-rs4765913) and the BD. No effect was encountered for cisgender men. Our model revealed that paths from CACNA1C SNPs to BD are mediated by specific temperament traits in women, reinforcing the definition of temperament traits as endophenotypes.

CD300f immunoreceptor is associated with major depressive disorder and decreased microglial metabolic fitness.

A role for microglia in neuropsychiatric diseases, including major depressive disorder (MDD), has been postulated. Regulation of microglial phenotype by immune receptors has become a central topic in many neurological conditions. We explored preclinical and clinical evidence for the role of the CD300f immune receptor in the fine regulation of microglial phenotype and its contribution to MDD. We found that a prevalent nonsynonymous single-nucleotide polymorphism (C/T, rs2034310) of the human CD300f receptor cytoplasmic tail inhibits the protein kinase C phosphorylation of a threonine and is associated with protection against MDD, mainly in women. Interestingly, CD300f-/- mice displayed several characteristic MDD traits such as augmented microglial numbers, increased interleukin 6 and interleukin 1 receptor antagonist messenger RNA, alterations in synaptic strength, and noradrenaline-dependent and persistent depressive-like and anhedonic behaviors in females. This behavioral phenotype could be potentiated inducing the lipopolysaccharide depression model. RNA sequencing and biochemical studies revealed an association with impaired microglial metabolic fitness. In conclusion, we report a clear association that links the function of the CD300f immune receptor with MDD in humans, depressive-like and anhedonic behaviors in female mice, and altered microglial metabolic reprogramming.

Genetic Variations in Elements of the Oxytocinergic Pathway are Associated with Attention/Hyperactivity Problems and Anxiety Problems in Childhood.

Genetic alterations related to oxytocin system seem to influence the neurobiology of attention-deficit hyperactivity disorder and anxiety problems leading to greater functional, social and emotional impairment. Here, we analyzed the association of OXTR rs2254298 and CD38 rs6449182 variants with attention/hyperactivity problems and anxiety problems in children. The study enrolled 292 children and adjusted regression model revealed OXTR rs2254298 AA genotype as a risk factor for attention deficit/hyperactivity problems (PR: 2.37; PadjFDR = 0.006), attention problems (PR: 2.71; PadjFDR = 0.003) and anxiety problems (PR: 1.92; PadjFDR = 0.018). CD38 rs6449182 G allele showed as a risk factor for attention deficit/hyperactivity problems (PR: 1.56; PadjFDR = 0.028). Moreover, in silico approach for regulatory roles found markers that influence chromatin accessibility and transcription capacity. Together, these data provide genetic information of oxytocin in developmental and behavioral disorders opening a range of opportunities for future studies that clarify their neurobiology in childhood.

Leptin polymorphism rs3828942: risk for anxiety disorders?

Leptin is an anorexigenic hormone well recognized by its role in mediating energy homeostasis. Recently, leptin has been associated with psychiatric disorders and interestingly, leptin treatment has shown antidepressant and anxiolytic effects. We examined the association of leptin levels and leptin (LEP) gene rs3828942 polymorphism with anxiety disorders considering sex differences. A cross-sectional population-based study, including 1067 young adults, of whom 291 presented anxiety disorders diagnosed by the Mini International Neuropsychiatric Interview (MINI 5.0). The rs3828942 polymorphism was genotyped by real-time PCR and ELISA measured leptin levels. Leptin levels were not associated with anxiety disorders after adjusting for sex and body mass index (BMI) [ß = - 0.009 (- 0.090-0.072); p = 0.832]. The distribution of rs3828942 genotypes was not associated with anxiety disorders. However, in a sex-stratified sample, the A-allele of rs3828942 polymorphism was associated with risk for GAD in women even when adjusting for confounding variables [OR = 1.87 (1.17-2.98); p = 0.008]. In a subsample of 202 individuals with GAD and control matched by sex and BMI, results suggest an interaction between genotypes and GAD diagnosis based on leptin levels only in the male group [F (1, 54) = 6.464; p = 0.0139]. Leptin is suggested to be related with the neurobiology of anxiety disorders in a sex-dependent manner since women carrying the A-allele of LEP rs3828942 present a higher risk for GAD, while leptin levels seem to be lower in men with GAD carrying A-allele. Studies on the relationship between leptin polymorphisms and levels are scarce and, therefore, further research is necessary.

Generalized Anxiety Disorder, Depressive Symptoms and the Occurrence of Stressors Events in a Probabilistic Sample of Pregnant Women.

The aim of the study is to verify the association between GAD, the severity of depressive symptoms and stressors in pregnant women between the first and second trimester. Cross-sectional study, part of a cohort that followed 980 women during the gestational period of a city in southern Brazil. We performed bivariate analysis using the t-test and chi-square. The variables that presented p ≤ 0.20 were taken for multivariate analysis, through logistic regression, in order to control possible confounding factors. The Mini International Neuropsychiatric Interview Plus was used to evaluate GAD, the severity of depressive symptoms was investigated through the Beck Inventory of Depression II, and stress events according to the Social Readjustment Assessment Scale of Holmes e Rahe. The sample consisted of 980 women. Women with mild depression symptoms had 9.8 (IC95% 4.6;21.0) times more GAD, those with moderate symptoms had 27.5 (IC95% 12.5;60.0) times more GAD, and those with severe symptoms had 52.9 (IC95% 19.1;146.5) times more GAD when compared to pregnant women with no symptoms or minimal symptoms. Regarding the stressful events, the pregnant women who presented GAD had an increase of 1.0 (IC95% 1.0;1.1) point in the mean of occurrence of stressor events when compared to those without GAD. These findings highlight the need for prevention strategies and interventions to promote maternal mental health, which benefit the development of infants in the long term.

Impact of genetic variations in ADORA2A gene on depression and symptoms: a cross-sectional population-based study.

Genetic variants involved in adenosine metabolism and its receptors were associated with increased risk for psychiatric disorders, including anxiety, depression, and schizophrenia. Here, we examined an association between a single nucleotide polymorphism in A2A receptor gene (ADORA2A, rs2298383 SNP) with current depressive episode and symptom profile. A total of 1253 individuals from a cross-sectional population-based study were analyzed by the Mini International Neuropsychiatric Interview 5.0. Our data showed that the TT genotype of ADORA2A rs2298383 SNP was associated with reduced risk for depression when compared to the CC/CT genotypes (p = 0.020). This association remained significant after adjusting for confounding variables such as smoking, gender, socioeconomic class, and ethnicity (OR = 0.631 (95% CI 0.425-0.937); p = 0.022). Regarding the symptoms associated with depression, we evaluated the impact of the ADORA2A SNP in the occurrence of sad/discouraged mood, anhedonia, appetite changes, sleep disturbances, motion changes, energy loss, feelings of worthless or guilty, difficulty in concentrating, and presence of bad thoughts. Notably, the TT genotype was independently associated with reduced sleep disturbances (OR = 0.438 (95% CI 0.258-0.743); p = 0.002) and less difficulty in concentrating (OR = 0.534 (95% CI 0.316-0.901; p = 0.019). The cross-sectional design cannot evaluate the cause-effect relationship and did not evaluate the functional consequences of this polymorphism. Our data support an important role for ADORA2A rs2298383 SNP in clinical heterogeneity associated with depression. The presence of the TT genotype was associated with decrease risk for current depression and disturbances in sleep and attention, two of the most common symptoms associated with this disorder.

Iodonium salt incorporation in dental adhesives and its relation with degree of conversion, ultimate tensile strength, cell viability, and oxidative stress.

OBJECTIVE: The aim of this study was to evaluate the degree of conversion, ultimate tensile strength, cell viability, and oxidative stress of two different ternary initiation systems, using two photoinitiation polymerization times. METHODS: The groups investigated were camphorquinone (CQ); CQ and diphenyleneiodonium hexafluorophosphate (DPI); CQ and ethyl 4-dimethylamine benzoate (EDAB); and CQ, EDAB, and DPI, with EDAB in high and low concentration. To assess the degree of conversion (DC) and the ultimate tensile strength (UTS), a real-time Fourier transform infrared spectroscopy and a universal test machine Emic DL-500 were used, respectively. Cell viability and oxidative stress were evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), superoxide dismutase (SOD), total sulfhydryl (SH) content, and thiobarbituric acid reactive species (TBARS) formation assays. RESULTS: Slight lower cell viability was shown when DPI was associated with high concentrations of EDAB; this reduction seemed to be attenuated when lower concentrations of EDAB were used. When EDAB and DPI were associated, no oxidative damage was shown. The degree of conversion was increased in the ternary systems (CQ + EDAB lower concentration + DPI) group, which did not affect the UTS, cytotoxicity, and oxidative stress parameters. The polymerization time did not affect cell viability, total SH, and TBARS; however, a slight increase was shown in SOD levels. CLINICAL RELEVANCE: Our study emphasizes the relevance of incorporating the third element-iodonium salt-in a binary adhesive systems composed exclusively of CQ and EDAB.

The role of CLOCK gene in psychiatric disorders: Evidence from human and animal research.

The circadian clock system drives daily rhythms in physiology, metabolism, and behavior in mammals. Molecular mechanisms of this system consist of multiple clock genes, with Circadian Locomotor Output Cycles Kaput (CLOCK) as a core member that plays an important role in a wide range of behaviors. Alterations in the CLOCK gene are associated with common psychiatric disorders as well as with circadian disturbances comorbidities. This review addresses animal, molecular, and genetic studies evaluating the role of the CLOCK gene on many psychiatric conditions, namely autism spectrum disorder, schizophrenia, attention-deficit/hyperactivity disorder, major depressive disorder, bipolar disorder, anxiety disorder, and substance use disorder. Many animal experiments focusing on the effects of the Clock gene in behavior related to psychiatric conditions have shown consistent biological plausibility and promising findings. In humans, genetic and gene expression studies regarding disorder susceptibility, sleep disturbances related comorbidities, and response to pharmacological treatment, in general, are in agreement with animal studies. However, the number of controversial results is high. Literature suggests that the CLOCK gene exerts important influence on these conditions, and influences the susceptibility to phenotypes of psychiatric disorders.

NLRP3 inflammasome-driven pathways in depression: Clinical and preclinical findings.

Over the past three decades, an intricate interaction between immune activation, release of pro-inflammatory cytokines and changes in brain circuits related to mood and behavior has been described. Despite extensive efforts, questions regarding when inflammation becomes detrimental or how we can target the immune system to develop new therapeutic strategies for the treatment of psychiatric disorders remain unresolved. In this context, novel aspects of the neuroinflammatory process activated in response to stressful challenges have recently been documented in major depressive disorder (MDD). The Nod-like receptor pyrin containing 3 inflammasome (NLRP3) is an intracellular multiprotein complex responsible for a number of innate immune processes associated with infection, inflammation and autoimmunity. Recent data have demonstrated that NLRP3 activation appears to bridge the gap between immune activation and metabolic danger signals or stress exposure, which are key factors in the pathogenesis of psychiatric disorders. In this review, we discuss both preclinical and clinical evidence that links the assembly of the NLRP3 complex and the subsequent proteolysis and release of the pro-inflammatory cytokines interleukin-1ß (IL-1ß) and interleukin-18 (IL-18) in chronic stress models and patients with MDD. Importantly, we also focus on the therapeutic potential of targeting the NLRP3 inflammasome complex to improve stress resilience and depressive symptoms.

Preventive Effect of Cecropia pachystachya Against Ketamine-Induced Manic Behavior and Oxidative Stress in Rats.

Cecropia species are widely used in traditional medicine by its anti-diabetic, anti-hypertensive and anti-inflammatory properties. In the present study, we investigated the neuroprotective and antioxidant effects of the crude aqueous extract from Cecropia pachystachya leaves in a rat model of mania induced by ketamine. The results indicated that ketamine treatment (25 mg/kg i.p., for 8 days) induced hyperlocomotion in the open-field test and oxidative damage in prefrontal cortex and hippocampus, evaluated by increased lipid peroxidation, carbonyl protein formation and decreased total thiol content. Moreover, ketamine treatment reduced the activity of the antioxidant enzymes superoxide dismutase and catalase in hippocampus. Pretreatment of rats with C. pachystachya aqueous extract (200 and 400 mg/kg p.o., for 14 days) or with lithium chloride (45 mg/kg p.o., for 14 days, used as a positive control) prevented both behavioral and pro-oxidant effects of ketamine. These findings suggest that C. pachystachya might be a useful tool for preventive intervention in bipolar disorder, reducing the episode relapse and the oxidative damage associated with the manic phase of this disorder .

Leptin in depressive episodes: is there a difference between unipolar and bipolar depression?

OBJECTIVE: The present study investigated whether peripheral leptin levels are associated with current depressive episodes in a cross-sectional study nested within a population-based study. METHODS: The Mini-International Neuropsychiatric Interview (MINI) 5.0 was used to assess the presence of current depressive episodes. The sample was composed of 206 subjects (103 controls and 103 subjects with a current depressive episode) paired by gender, BMI and age. Medication use and lifestyle characteristics were self-reported. RESULTS: Serum leptin levels were lower in currently depressive subjects (10.9 ± 12.0 ng/ml) than in the control group (20.3 ± 24.0 ng/ml; p = 0.023). According to the clinical diagnosis, individuals with bipolar depression present lower leptin levels (8.4 ± 8.1 ng/ml) than those with unipolar depression (12.0 ± 13.4 ng/ml) and the control group (20.3 ± 24.0 ng/ml; p = 0.031). In addition, ANCOVA showed that leptin is an independent factor associated with current depressive episodes (p = 0.018). CONCLUSION: A decreased leptin level might be a useful peripheral marker associated with depressive episodes in the context of bipolar disorder.

Elodontoma in Two Guinea Pigs.

Elodontoma was diagnosed in two pet guinea pigs, one involving a maxillary premolar tooth and the other affecting a mandibular incisor tooth. Diagnostic imaging, including radiographs, computed tomography, and oral endoscopy was performed in order to quantify dental disease. Diagnostic imaging was also used to guide treatment of acquired dental disease, which included intraoral restoration of normal occlusal plane and tooth extraction using an extraoral approach. These are the first histologically confirmed cases of elodontoma in guinea pigs.

Immune dysfunction in bipolar disorder and suicide risk: is there an association between peripheral corticotropin-releasing hormone and interleukin-1ß?

OBJECTIVE: The aim of the present study was to investigate the relationship between peripheral levels of corticotropin-releasing hormone (CRH) and interleukin-1ß (IL-1ß) in individuals with bipolar disorder (BD) with and without suicide risk (SR), and controls. METHODS: A total of 120 young adults (40 controls, 40 subjects with BD without SR, and 40 subjects with BD with SR) were enrolled from a population-based study carried out in the city of Pelotas, Brazil. BD and SR were assessed through the Mini International Neuropsychiatric Interview (MINI 5.0), and peripheral markers were evaluated by enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of CRH were significantly lower both in subjects with BD without SR (p = 0.04) and subjects with BD with SR (p = 0.02) when compared to controls. However, levels of IL-1ß were increased in subjects with BD with SR (p = 0.05) when compared to controls. Sociodemographic and clinical variables, current mood episode, and use of psychiatric medications were not associated with changes in these markers. No correlation was found between peripheral levels of CRH and IL-1ß (p = 0.60) in the population or in the BD with SR group (p = 0.88). CONCLUSIONS: These results suggest that peripheral mechanisms linking stress hormones and the immune system might be critical patterns involved in suicidal behavior associated with BD.

Cytology of a seminoma in a koi (Cyprinus carpio): a rapid diagnostic tool.

Koi(Cyprinus carpio) is an ornamental variety of common carp frequently kept as pets. Given their long lifespan, neoplasia, albeit uncommon, may occur in these animals, and only a few studies have faced their cytological diagnosis. In the present case, a koi carp was referred to the clinicians due to coelomic swelling. The carp underwent surgery, which revealed an enlargement of both testes. Testicular samples were cytologically and histologically examined. The lesion was diagnosed as a seminoma since it was composed of round, large, atypical, and often multinucleated cells with round central nuclei and moderate cytoplasm. These tumors had the same appearance as seminomas in mammals and should be considered among differential diagnoses when coelomic swelling occurs in koi carp. Seminomas in koi carp are diagnosed histologically, but cytology, a rapid and cheap exam executable in all veterinary clinical facilities, could be a relevant preliminary diagnostic tool that may influence the entire diagnostic process.

Amygdala-specific changes in Cacna1c, Nfat5, and Bdnf expression are associated with stress responsivity in mice: A possible mechanism for psychiatric disorders.

The CACNA1C gene encodes the alpha-1c subunit of the Cav1.2 calcium channel, a regulator of neuronal calcium influx involved in neurotransmitter release and synaptic plasticity. Genetic data show a role for CACNA1C in depressive symptoms underlying different psychiatric diagnoses. However, the mechanisms involved still require further exploration. This study aimed to investigate sex and region-specific changes in the Cacna1c gene and behavioral outcomes in mice exposed to chronic stress. Moreover, we evaluated the Nuclear factor of activated T-cells 5 (Nfat5) and the Brain-derived neurotrophic factor (Bdnf) as potential upstream and downstream Cacna1c targets and their correlation in stressed mice and humans with depression. Male and female Swiss mice were exposed to chronic unpredictable stress (CUS) for 21 days. Animal-integrated emotionality was assessed using the sucrose splash test, the tail suspension, the open-field test, and the elevated-plus-maze. Gene expression analysis was performed in the amygdala, prefrontal cortex, and hippocampus. Human data for in silico analysis was obtained from the Gene Expression Omnibus. CUS-induced impairment in integrated emotional regulation was observed in males. Gene expression analysis showed decreased levels of Cacna1c and Nfat5 and increased levels of Bdnf transcripts in the amygdala of stressed male mice. In contrast, there were no major changes in behavioral responses or gene expression in female mice after stress. The expression of the three genes was significantly correlated in the amygdala of mice and humans. The strong and positive correlation between Canac1c and Nfat5 suggests a potential role for this transcription factor in Canac1c expression. These changes could impact amygdala reactivity and emotional responses, making them a potential target for psychiatric intervention.

Maternal hsa-miR-423-5p associated with the cognitive development of babies in pregnant women without mental disorders.

Background: MicroRNAs (miRNAs) are small non-coding RNAs capable of regulating gene expression post-transcriptionally. MiRNAs are recognized as key regulators of diverse biological and developmental processes. During the pregnancy-puerperal cycle, numerous changes occur in the female body for the formation, growth, and development of the baby. After birth, there is a critical period in child development, as rapid gains in the physical, cognitive, and socio-emotional domains constitute the "building blocks" of children's later growth. Objective: The aim of this study was to investigate the association between maternal expression of hsa-miR-423-5p during the first and second trimesters of pregnancy and neurocognitive development at 90 days of life in infants. Methods: This is a longitudinal study included in a population-based cohort study, carried out in a city in southern Brazil. The Bayley III was used to assess the babies' cognitive development. Blood samples from mothers were obtained for RNA extraction from serum and analysis of miRNA expression by qRT-PCR. Results: In total, 87 dyads (mother-baby) were included. The average gestational age was 15.86 weeks (SD ± 5.55). An association of maternal miRNA with infant cognitive development was found; as maternal miR-423-5p increases, infants' cognitive development increases by 2.40 (95% CI 0.37; 4.43, p = 0.021) points at 3 months of age. Conclusion: In this context, it is suggested to use this miRNA as a biomarker of child neurocognitive development detectable in the prenatal period, thus allowing the planning of early interventions.

Selenium compounds prevent amyloid ß-peptide neurotoxicity in rat primary hippocampal neurons.

Neuropathological hallmarks of Alzheimer's disease (AD) include amyloid plaque formation, neurofibrillary tangles, neuronal and synaptic loss. This study aims to identify the neuroprotective effects of the selenium compounds on the neurotoxicity of amyloid ß(1-42) in primary cultures of murine hippocampal neurons. Samples were subjected to immunocytochemistry and western blotting techniques to determine the role of treatments on neuronal viability and synaptic protein SNAP-25. We observed a reduced cell viability amyloid ß-peptide (1-42)-induced. When cells were co-treated with amyloid ß-peptide (1-42) and selenium compounds, we verified a strong increase in relative cell viability and in the level of synaptic marker synaptosomal-associated protein SNAP-25 induced by selenium compounds.

Reduced serum levels of neuron specific enolase (NSE) in drug-naïve subjects with major depression and bipolar disorder.

Several biological factors have been recently related with major depression and bipolar disorder. The aim of our paper was to investigate the peripheral levels of the protein neuronal specific enolase (NSE), a putative marker of neuronal damage, comparing patients with major depressive disorder and bipolar disorder to control subjects. This is a case-control study nested in a cross-sectional population-based survey. Psychopathology screen was performed using the Mini-International Neuropsychiatric Interview 5.0 and blood samples were collected from 108 young adults. Three groups were selected, 36 healthy controls, 36 subjects with major depression disorder and 36 subjects with bipolar disorder. Serum levels of NSE significantly decreased (p = 0.002) in major depression disorder (2.19 ± 1.78 ng/mL) and bipolar disorder subjects (2.53 ± 2.61 ng/mL) compared to the control group (3.55 ± 2.19 ng/mL). In conclusion, peripheral neuronal specific enolase may be a useful marker drug-naïve major depression disorder and bipolar disorder, but its pathophysiological significance and response to treatment should be further investigated.

Primary intranasal perivascular wall tumors in 2 cats.

Perivascular wall tumors (PWTs) are common well-known canine mesenchymal tumors. The term PWT has not yet been applied to cats; only 2 cases of feline soft tissue hemangiopericytomas (HEPs) are available. In human medicine, sinonasal HEP-like tumor/glomangiopericytoma (SHPCL/GP) and intranasal solitary fibrous tumor (SFT) are well-known mesenchymal tumors with staghorn vasculature and low malignant potential; however, these entities have not been described in small animals. We describe here the pathologic and immunohistochemical features of 2 cases of feline intranasal mesenchymal tumors consistent with PWTs and resembling human SHPCL/GP (case 1), and human intranasal SFT (case 2). Both cats developed intranasal, unilateral, polypoid, expansile neoplasms with a mostly patternless growth of spindle cells, minimal stroma, and prominent staghorn vessels. The stroma was PAS negative, which excludes a glomus tumor. Immunohistochemistry identified diffuse vimentin and PDGFRß expression. Case 1 was α-SMA positive (as is human SHPCL/GP); case 2 was negative (as is human intranasal SFT). Both tumors were incompletely excised, leading to recurrence in case 1. Case 2 was lost to follow up. To our knowledge, intranasal PWTs have not been reported previously in cats. The frequency of the lesions is not known, but awareness of these entities may assist in their recognition and better characterization in the future.