PeerJ Preprints: Pathologyhttps://peerj.com/preprints/index.atom?journal=peerj&subject=6100Pathology articles published in PeerJ PreprintsMultifaceted role of tensins in cancerhttps://peerj.com/preprints/279902019-09-272019-09-27Abdulaziz AlfahedTeresa P RaposoMohammad Ilyas
Tensins are structural adaptor proteins localized at focal adhesions. Tensins can act as mechanosensors and participate in the transduction of biochemical signals from the extracellular matrix to the cytoskeleton, acting as an interface able to alter cell behavior in responses to changes in their surrounding environment. This review aims to provide a concise summary of the main functions of the four known tensins in cell and cancer biology, their homology and recently unveiled signaling mechanisms. We focus specifically on how tensin 4 (TNS4/Cten) may contribute to cancer both as an oncogene supporting metastasis and as tumour suppressor in different types of tissue. A better understanding of the cancer mechanistics involving tensins may provide the rationale for development of specific therapeutic strategies.
Tensins are structural adaptor proteins localized at focal adhesions. Tensins can act as mechanosensors and participate in the transduction of biochemical signals from the extracellular matrix to the cytoskeleton, acting as an interface able to alter cell behavior in responses to changes in their surrounding environment. This review aims to provide a concise summary of the main functions of the four known tensins in cell and cancer biology, their homology and recently unveiled signaling mechanisms. We focus specifically on how tensin 4 (TNS4/Cten) may contribute to cancer both as an oncogene supporting metastasis and as tumour suppressor in different types of tissue. A better understanding of the cancer mechanistics involving tensins may provide the rationale for development of specific therapeutic strategies.Identification of key gene modules and genes in colorectal cancer by weighted gene co-expression network analysis (WGCNA)https://peerj.com/preprints/276672019-04-192019-04-19Zheying ZhangNa LiQingzu GaoXinlai Qian
Background: Colorectal cancer (CRC) is a malignant tumor particularly common in developing countries. In this study, we used Weighted Gene Co-Expression Network Analysis (WGCNA) of chip data and screened hub genes in CRC to find the gene modules specifically correlated with clinical traits. Methods: WGCNA was used to identify the gene modules specifically associated with metastasis in colorectal cancer. Cytoscape software was used to construct a co-expression network. The expression of CYTH1 was determined by qRT-PCR. Results: Based on the predicted co-expression network, we identified that the turquoise module was associated with CRC clinical metastasis traits. Turquoise module genes were analyzed, and we identified the hub gene CYTH1 using Cytoscape software. Additionally, we found CYTH1’s expression was lower in CRC tissue and cells when compared with normal counterparts.
Background: Colorectal cancer (CRC) is a malignant tumor particularly common in developing countries. In this study, we used Weighted Gene Co-Expression Network Analysis (WGCNA) of chip data and screened hub genes in CRC to find the gene modules specifically correlated with clinical traits. Methods: WGCNA was used to identify the gene modules specifically associated with metastasis in colorectal cancer. Cytoscape software was used to construct a co-expression network. The expression of CYTH1 was determined by qRT-PCR. Results: Based on the predicted co-expression network, we identified that the turquoise module was associated with CRC clinical metastasis traits. Turquoise module genes were analyzed, and we identified the hub gene CYTH1 using Cytoscape software. Additionally, we found CYTH1’s expression was lower in CRC tissue and cells when compared with normal counterparts.Roles of pyroptosis in myocardial ischemia/reperfusion injury diseaseshttps://peerj.com/preprints/275022019-01-252019-01-25Shupeng ShiHaoran ZhangWenzhe GaoMoussa Ide NasserJie ShenMinghua YangFeng GuoLinyong XuMingyi Zhao
Ischemia-reperfusion injury (IRI) occurred when an organ lost its blood supply in a short time, and then the perfusion was restored automatically or iatrogenically, leading to a burst of reactive oxygen species (ROS) from mitochondria. It is common in the clinic, and lead to deterioration, even death, so an exploratory examination of the mechanism of ischemia-reperfusion injury is of great significance. Among the most common and fatal types of IR in myocardial tissue, myocardial IRI is one of the most fatal diseases in the modern world. The cellular and molecular mechanisms of IRI mainly include calcium overload, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, energy metabolic disorders, neutrophil infiltration, cardiomyocyte autophagy, and apoptosis, etc. The main pathogenesis of IRI is programmed cell death, of which apoptosis is the most deeply studied processes. However, pyroptosis is a highly inflammatory form of programmed cell death (PCD), which depends on the activation of the caspase cascade and inflammatory mediators, which have been thought to be involved in the processes of IRI. Ptosis has been referred to as a pattern. PCD with apoptosis characteristics Necrosis. It’s stimulated by molecular signaling pathways similar to apoptosis, mainly including Caspase. The research progress in recent years is presented in this review. Among them, myocardial tissue and so on provide a theoretical basis for the burning organ system in I/R injury and provide theoretical practice for the clinical research of reducing ischemia-reperfusion injury.
Ischemia-reperfusion injury (IRI) occurred when an organ lost its blood supply in a short time, and then the perfusion was restored automatically or iatrogenically, leading to a burst of reactive oxygen species (ROS) from mitochondria. It is common in the clinic, and lead to deterioration, even death, so an exploratory examination of the mechanism of ischemia-reperfusion injury is of great significance. Among the most common and fatal types of IR in myocardial tissue, myocardial IRI is one of the most fatal diseases in the modern world. The cellular and molecular mechanisms of IRI mainly include calcium overload, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, energy metabolic disorders, neutrophil infiltration, cardiomyocyte autophagy, and apoptosis, etc. The main pathogenesis of IRI is programmed cell death, of which apoptosis is the most deeply studied processes. However, pyroptosis is a highly inflammatory form of programmed cell death (PCD), which depends on the activation of the caspase cascade and inflammatory mediators, which have been thought to be involved in the processes of IRI. Ptosis has been referred to as a pattern. PCD with apoptosis characteristics Necrosis. It’s stimulated by molecular signaling pathways similar to apoptosis, mainly including Caspase. The research progress in recent years is presented in this review. Among them, myocardial tissue and so on provide a theoretical basis for the burning organ system in I/R injury and provide theoretical practice for the clinical research of reducing ischemia-reperfusion injury.Reusing microarray clinical data from a complex disease with bioinformatics toolhttps://peerj.com/preprints/273982018-11-302018-11-30Eugenio Del PreteAngelo FacchianoPietro Liò
Clinical bioinformatics, translational bioinformatics and personalised medicine are connected by the common task of analysing and integrating clinical data and results, in order to find important biomarkers related to pathologies and facilitate their prediction, diagnosis and treatment. New technologies provides the possibility to have more and more clinical data available in online databases. This data can be reused for studying complex disease from novel point of views. This work show how it is possible considering online microarray data from coeliac disease and some of its comorbidities, combining both the data and the results. The main goal is the extraction of common evidences among the selected pathologies, from genes to different kinds of functional annotation, showing which biological processes are more involved in these autoimmune disorders and quantifying the similarity between coeliac disease and its comorbidities. The pipeline of the work is developed in R language, and it is semi-automated. Methodologically, the advantage of this work is the possibility of performing the entire analysis starting from a different pathology; clinically, scientists can have the possibility of using data already published to highlight old and new evidences, with the possibility of improve the knowledge on a complex disease according to the availability of new microarray data.
Clinical bioinformatics, translational bioinformatics and personalised medicine are connected by the common task of analysing and integrating clinical data and results, in order to find important biomarkers related to pathologies and facilitate their prediction, diagnosis and treatment. New technologies provides the possibility to have more and more clinical data available in online databases. This data can be reused for studying complex disease from novel point of views. This work show how it is possible considering online microarray data from coeliac disease and some of its comorbidities, combining both the data and the results. The main goal is the extraction of common evidences among the selected pathologies, from genes to different kinds of functional annotation, showing which biological processes are more involved in these autoimmune disorders and quantifying the similarity between coeliac disease and its comorbidities. The pipeline of the work is developed in R language, and it is semi-automated. Methodologically, the advantage of this work is the possibility of performing the entire analysis starting from a different pathology; clinically, scientists can have the possibility of using data already published to highlight old and new evidences, with the possibility of improve the knowledge on a complex disease according to the availability of new microarray data.Genetic inactivation of alpha-synuclein affects embryonic development of dopaminergic neurons of the substantia nigra, but not the ventral tegmental area, in mouse brainhttps://peerj.com/preprints/265472018-05-102018-05-10Tatiana V TarasovaOlga A LytkinaValeria V GoloborshchevaLarisa N SkuratovskayaAlexandr I AntohinRuslan K OvchinnikovMichail S Kukharsky
Lesion of the dopaminergic neurons of the nigrostriatal system is a key feature of Parkinson's disease (PD). Alpha-synuclein is a protein that is a major component of Lewy bodies, histopathological hallmarks of PD, and is involved in regulation of dopamine (DA) neurotransmission. Previous studies of knockout mice have shown that inactivation of alpha-synuclein gene can lead to the reduction in number of DA neurons in the substantia nigra (SN). DA neurons of the SN are known to be the most affected in PD patients whereas DA neurons of neighboring ventral tegmental area (VTA) are much less susceptible to degeneration. Here we have studied the dynamics of changes in TH-positive cell numbers in the SN and VTA during a critical period of their embryonic development in alpha-synuclein knockout mice. This precise study of DA neurons during development of the SN revealed that not only is the number of DA neurons reduced by the end of the period of ontogenic selection, but that the way these neurons are formed is altered in alpha-synuclein knockout mice. At the same time, DA neurons in the VTA are not affected. Alpha-synuclein exerts a modulating effect on the formation of DA neurons in the SN and has no effect on the formation of DA neurons in VTA, the structure that is much less susceptible to degeneration in PD brain, suggesting a potential role of alpha-synuclein in the development of the population of DA neurons in substantia nigra.
Lesion of the dopaminergic neurons of the nigrostriatal system is a key feature of Parkinson's disease (PD). Alpha-synuclein is a protein that is a major component of Lewy bodies, histopathological hallmarks of PD, and is involved in regulation of dopamine (DA) neurotransmission. Previous studies of knockout mice have shown that inactivation of alpha-synuclein gene can lead to the reduction in number of DA neurons in the substantia nigra (SN). DA neurons of the SN are known to be the most affected in PD patients whereas DA neurons of neighboring ventral tegmental area (VTA) are much less susceptible to degeneration. Here we have studied the dynamics of changes in TH-positive cell numbers in the SN and VTA during a critical period of their embryonic development in alpha-synuclein knockout mice. This precise study of DA neurons during development of the SN revealed that not only is the number of DA neurons reduced by the end of the period of ontogenic selection, but that the way these neurons are formed is altered in alpha-synuclein knockout mice. At the same time, DA neurons in the VTA are not affected. Alpha-synuclein exerts a modulating effect on the formation of DA neurons in the SN and has no effect on the formation of DA neurons in VTA, the structure that is much less susceptible to degeneration in PD brain, suggesting a potential role of alpha-synuclein in the development of the population of DA neurons in substantia nigra.Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric studyhttps://peerj.com/preprints/265102018-02-122018-02-12Emoke HorvathAlex OradanLiviu ChiriacMinodora DobreanuElőd-Ernő NagyAdina Hutanu
Background and Objective: Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model.
Methods: Fifteen adult Wistar male rats were divided randomly into test (n=10) and sham (n=5) groups. In the ischemic group, transient focal cerebral ischemia was induced with an intraluminal filament technique. Histologic lesions of the ischemic core and the surrounding penumbra zone were evaluated, based on a complex algorithm. Representative morphological changes in the core and the penumbra zone were compared. Immunohistochemistry was performed for leukocytes markers (CD15, CD68, CD3), leukocyte-released effectors (MMP-9 and COX-2), and FXIII (possibly involved in microglia and macrophage activation)
Results: Neuronal vacuolation and degeneration were significantly more in the core lesion, whereas cellular edema and inflammatory infiltrate were increased in the penumbra. CD68, CD3, FXIII and Cox-2 expression were significantly higher in the penumbra than in the core (p=0.026; p=0.006; p=0.002; and p<0.001).
Discussion: In the rat model of middle cerebral artery occlusion, inflammatory mechanisms, microglia/macrophage cells, and T-lymphocytes likely play an important role in the penumbra. The deterioration of neurons is less in the penumbra than in the core. Appreciation of the role of the inflammatory cells and mechanisms involved in stroke might lead to measures to inhibit the injury and save brain volume.
Background and Objective: Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model.Methods: Fifteen adult Wistar male rats were divided randomly into test (n=10) and sham (n=5) groups. In the ischemic group, transient focal cerebral ischemia was induced with an intraluminal filament technique. Histologic lesions of the ischemic core and the surrounding penumbra zone were evaluated, based on a complex algorithm. Representative morphological changes in the core and the penumbra zone were compared. Immunohistochemistry was performed for leukocytes markers (CD15, CD68, CD3), leukocyte-released effectors (MMP-9 and COX-2), and FXIII (possibly involved in microglia and macrophage activation)Results: Neuronal vacuolation and degeneration were significantly more in the core lesion, whereas cellular edema and inflammatory infiltrate were increased in the penumbra. CD68, CD3, FXIII and Cox-2 expression were significantly higher in the penumbra than in the core (p=0.026; p=0.006; p=0.002; and p<0.001).Discussion: In the rat model of middle cerebral artery occlusion, inflammatory mechanisms, microglia/macrophage cells, and T-lymphocytes likely play an important role in the penumbra. The deterioration of neurons is less in the penumbra than in the core. Appreciation of the role of the inflammatory cells and mechanisms involved in stroke might lead to measures to inhibit the injury and save brain volume.Histological and histochemical investigation of the compound eye of the whiteleg shrimp (Litopenaeus vannamei)https://peerj.com/preprints/34532017-12-082017-12-08Hao-Kai ChangCheng-Chung LinShih-Ling Hsuan
The compound eye is the primary visual system in crustaceans. Although the histological structure and histochemical characteristics of compound eyes of some insect and crab species are now well understood, no such studies have been undertaken in the whiteleg shrimp (Litopenaeus vannamei). In this study, eye samples from L. vannamei were fixed and paraffin sections were stained using several histochemical methods. The histological structure of each layer of the compound eye was examined and compared using different histochemical staining methods. It was found that the compound eye of L. vannamei consisted of cuticle, cornea, ommatidia, optic nerve layer, lamina ganglionaris, and medulla in an outside-in order. The cuticle of L. vannamei eyes was very thin, composed of a single epicuticle layer, as confirmed by Masson’s trichrome stain. The screening pigments produced by screening pigment cells were arranged at the junction of the ommatidia and optic nerve layer; these pigments stained differentially after different histochemical staining methods suggesting the screening pigment cells can be classified into different types. Notably, clusters of foamy glandular cells (FGCs) were observed in the optic nerve layer; these stained positively with periodic acid-Schiff and toluidine blue, and appeared blue after Masson’s trichrome stain. Immunohistochemical (IHC) staining was used to further define the origin and characteristics of FGCs. The IHC analysis showed that FGCs were positive for vimentin and synaptophysin (SYN), suggesting their neuroendocrine nature. In the medulla internalis and medulla terminalis, the neural clusters that surround the neurophil could be divided into three types by differences in morphology: the largest and the smallest cell clusters were neuron clusters and neurosecretory cells, respectively; the middle-sized cell clusters appeared SYN-positive and have not previously been described. Overall, this study is the first to provide a detailed description of the normal features of the compound eye of L. vannamei. The identification of different types of screening pigments in the ommatidia, the endocrine nature of FGcs in the optic nerve layer, and the novel neural clusters between the medulla internalis and medulla terminalis, will be important information for further study into the compound eye of L. vannamei.
The compound eye is the primary visual system in crustaceans. Although the histological structure and histochemical characteristics of compound eyes of some insect and crab species are now well understood, no such studies have been undertaken in the whiteleg shrimp (Litopenaeus vannamei). In this study, eye samples from L. vannamei were fixed and paraffin sections were stained using several histochemical methods. The histological structure of each layer of the compound eye was examined and compared using different histochemical staining methods. It was found that the compound eye of L. vannamei consisted of cuticle, cornea, ommatidia, optic nerve layer, lamina ganglionaris, and medulla in an outside-in order. The cuticle of L. vannamei eyes was very thin, composed of a single epicuticle layer, as confirmed by Masson’s trichrome stain. The screening pigments produced by screening pigment cells were arranged at the junction of the ommatidia and optic nerve layer; these pigments stained differentially after different histochemical staining methods suggesting the screening pigment cells can be classified into different types. Notably, clusters of foamy glandular cells (FGCs) were observed in the optic nerve layer; these stained positively with periodic acid-Schiff and toluidine blue, and appeared blue after Masson’s trichrome stain. Immunohistochemical (IHC) staining was used to further define the origin and characteristics of FGCs. The IHC analysis showed that FGCs were positive for vimentin and synaptophysin (SYN), suggesting their neuroendocrine nature. In the medulla internalis and medulla terminalis, the neural clusters that surround the neurophil could be divided into three types by differences in morphology: the largest and the smallest cell clusters were neuron clusters and neurosecretory cells, respectively; the middle-sized cell clusters appeared SYN-positive and have not previously been described. Overall, this study is the first to provide a detailed description of the normal features of the compound eye of L. vannamei. The identification of different types of screening pigments in the ommatidia, the endocrine nature of FGcs in the optic nerve layer, and the novel neural clusters between the medulla internalis and medulla terminalis, will be important information for further study into the compound eye of L. vannamei.A novel animal model for neuroinflammation and white matter degenerationhttps://peerj.com/preprints/31172017-08-012017-08-01Baohu JiKerin HigaVirawudh SoontornniyomkijAtsushi MiyanoharaXianjin Zhou
Small interference RNA has been widely used to suppress gene expression. Three different short-hairpin RNAs (shRNAs) against dopamine D1 receptor (Drd1), driven by mouse U6 promoter in self-complementary AAV8 vector (scAAV8), were used to silence mouse striatal Drd1 expression. Transduction of mouse striatum with all 3 scAAV8-D1shRNA virus, but not the control scAAV8 virus, causes extensive neuroinflammation, demyelination, and axon degeneration. RNA interference is known to be coupled to the innate immune system as a host cell defense against virus infection. Activation of the innate immune system may play a causal role in the development of neuroinflammation and white matter degeneration, providing a novel animal model for multiple sclerosis (MS) and other neuroinflammatory diseases.
Small interference RNA has been widely used to suppress gene expression. Three different short-hairpin RNAs (shRNAs) against dopamine D1 receptor (Drd1), driven by mouse U6 promoter in self-complementary AAV8 vector (scAAV8), were used to silence mouse striatal Drd1 expression. Transduction of mouse striatum with all 3 scAAV8-D1shRNA virus, but not the control scAAV8 virus, causes extensive neuroinflammation, demyelination, and axon degeneration. RNA interference is known to be coupled to the innate immune system as a host cell defense against virus infection. Activation of the innate immune system may play a causal role in the development of neuroinflammation and white matter degeneration, providing a novel animal model for multiple sclerosis (MS) and other neuroinflammatory diseases.lncRNA H19 mediates TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT Signaling Pathwayhttps://peerj.com/preprints/30892017-07-172017-07-17wei yangxuezhong lishaopei qixueru likun zhousuzhu qingyong zhangMingqing Gao
Increased levels of long noncoding RNA H19 (H19) have been observed in many inflammatory and organ fibrosis diseases including ulcerative colitis, osteoarthritis, liver fibrosis, renal fibrosis and pulmonary fibrosis. However, the role of H19 in bovine mastitis and mastitis-caused fibrosis is still unclear. In our study, H19 was characterized as a novel regulator of EMT induced by transforming growth factor-β1 (TGF-β1) in bovine mammary alveolar cell-T (MAC-T) cell line. We found that H19 was highly expressed in bovine mastitis tissues and inflammatory MAC-T cells induced by virulence factors of pathogens. TGF-β1 was also highly expressed in inflammatory MAC-T cells, and exogenous TGF-β1 could induce EMT, enhance extracellular matrix protein expression, and upregulate H19 expression in epithelial cells. Stable expression of H19 significantly promotes EMT progression and expression of ECM protein induced by TGF-β1 in MAC-T cells. Furthermore, by using a specific inhibitor of the PI3K/AKT pathway, we demonstrated that TGF-β1 upregulated H19 expression through PI3K/AKT pathway. All these observations imply that the lncRNA H19 modulated TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT signaling pathway, which suggests that mammary epithelial cells might be one source for myofibroblasts in vivo in the mammary glands under an inflammatory condition, thereby contributing to mammary gland fibrosis.
Increased levels of long noncoding RNA H19 (H19) have been observed in many inflammatory and organ fibrosis diseases including ulcerative colitis, osteoarthritis, liver fibrosis, renal fibrosis and pulmonary fibrosis. However, the role of H19 in bovine mastitis and mastitis-caused fibrosis is still unclear. In our study, H19 was characterized as a novel regulator of EMT induced by transforming growth factor-β1 (TGF-β1) in bovine mammary alveolar cell-T (MAC-T) cell line. We found that H19 was highly expressed in bovine mastitis tissues and inflammatory MAC-T cells induced by virulence factors of pathogens. TGF-β1 was also highly expressed in inflammatory MAC-T cells, and exogenous TGF-β1 could induce EMT, enhance extracellular matrix protein expression, and upregulate H19 expression in epithelial cells. Stable expression of H19 significantly promotes EMT progression and expression of ECM protein induced by TGF-β1 in MAC-T cells. Furthermore, by using a specific inhibitor of the PI3K/AKT pathway, we demonstrated that TGF-β1 upregulated H19 expression through PI3K/AKT pathway. All these observations imply that the lncRNA H19 modulated TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT signaling pathway, which suggests that mammary epithelial cells might be one source for myofibroblasts in vivo in the mammary glands under an inflammatory condition, thereby contributing to mammary gland fibrosis.Are anti-ganglioside antibodies associated with proventricular dilatation disease in birds?https://peerj.com/preprints/28522017-03-062017-03-06Jeann Leal de AraujoIan TizardJianhua GuoJ Jill HeatleyAline Rodrigues HoffmannRaquel R Rech
The identification of Parrot bornaviruses in psittacine birds with proventricular dilatation disease (PDD) has not been sufficient to explain the pathogenesis of this fatal disease since not all infected birds develop clinical signs. One hypothesis suggests that PaBV could trigger the production of autoantibodies targeting neuronal gangliosides. These are major neuronal antigens, and PDD might therefore resemble Guillain-Barré Syndrome (GBS) in its pathogenesis. Experimental inoculation of pure gangliosides and brain-derived ganglioside extracts were used in two different immunization studies. A preliminary study on seven healthy chickens (Gallus gallus domesticus) was performed using a group of four chickens inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and a control group comprised by three chickens inoculated only with phosphate-buffered saline (PBS). A second study with five healthy quaker parrots (Myiopsitta monachus) was comprised of three groups. Two quaker parrots received purified gangliosides in FCA, two received a crude brain extract in FCA, and one control quaker parrot received FCA alone. In the preliminary study, one chicken developed ataxia and weakness. None of the quaker parrots had any clinical signs that could resemble PDD or GBS. None of the chickens or quaker parrots presented any gross lesions. The chicken with clinical signs had a perivascular and perineural lymphocytic infiltrate in the proventriculus. Two of the quaker parrots (one from each treatment group) developed mild lymphoplasmacytic encephalitis and myelitis. Our results suggest that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD.
The identification of Parrot bornaviruses in psittacine birds with proventricular dilatation disease (PDD) has not been sufficient to explain the pathogenesis of this fatal disease since not all infected birds develop clinical signs. One hypothesis suggests that PaBV could trigger the production of autoantibodies targeting neuronal gangliosides. These are major neuronal antigens, and PDD might therefore resemble Guillain-Barré Syndrome (GBS) in its pathogenesis. Experimental inoculation of pure gangliosides and brain-derived ganglioside extracts were used in two different immunization studies. A preliminary study on seven healthy chickens (Gallus gallus domesticus) was performed using a group of four chickens inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and a control group comprised by three chickens inoculated only with phosphate-buffered saline (PBS). A second study with five healthy quaker parrots (Myiopsitta monachus) was comprised of three groups. Two quaker parrots received purified gangliosides in FCA, two received a crude brain extract in FCA, and one control quaker parrot received FCA alone. In the preliminary study, one chicken developed ataxia and weakness. None of the quaker parrots had any clinical signs that could resemble PDD or GBS. None of the chickens or quaker parrots presented any gross lesions. The chicken with clinical signs had a perivascular and perineural lymphocytic infiltrate in the proventriculus. Two of the quaker parrots (one from each treatment group) developed mild lymphoplasmacytic encephalitis and myelitis. Our results suggest that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD.