Immunodistribution of amyloid beta protein (Aβ) and advanced glycation end-product receptors (RAGE) in choroid plexus and ependyma of resuscitated patients

RAGE (receptor for advanced glycation end-products) participates in the influx transport of glycated Aβ (amyloid beta) from the blood to the brain. Because little is known of the RAGE operating in brain barriers such as those in the choroid plexus and ependyma, the aim of the present study was to examine the immunodistributions of RAGE and Aβ peptides in the choroid plexus where the blood-cerebrospinal fluid barrier (B-CSF) is located, and in ependyma of the brain ventricles associated with functions of the cerebrospinal fluid-brain barrier (CSF-B). The study was performed on patients over 65 years successfully resuscitated after cardiac arrest with survival a few weeks. The control group consisted of age-matched individuals who were not resuscitated and died immediately after cardiac arrest. In resuscitated patients, but not in controls, RAGE receptors were localized in choroid plexus (CP) epithelial cells and in ependymal cells bordering the brain ventricles. These cells form the B-CSF and CSF-B barriers. The presence of Aβ was detected within the CP blood vessels and in the basement membrane of the CP epithelium. In numerous cytoplasmic vacuoles of CP epithelial and ependymal cells Aβ protein was found and our observations suggest that the contents of those vacuoles were undergoing progressive digestion. The results demonstrated that CP epithelium and ependymal cells, equipped with RAGE receptors, not only play an important role in the creation of amyloid deposits in the brain but are also places where Aβ may be utilized. The RAGE transportation system should be a main target in the therapy of brain amyloidosis, a well-known risk factor of Alzheimer disease.     

Focal ependymal differentiation in choroid plexus papillomas

Summary Choroid plexus papillomas are usually easily distinguishable from papillary ependymomas by their delicate fibrovascular stroma and their cytologic similarity to normal choroid plexus epithelium. Exceptionally, however, examples are met which give rise to diagnostic difficulty. We therefore tested 22 choroid plexus papillomas for the presence of glial fibrillary acidic (GFA) protein using the immunoperoxidase technique. Positivity for the protein was found focally in epithelial tumor cells in nine of the 22 papillomas. All were in adults ranging from 19–66 years of age. Eight of the nine tumors originated in the 4th ventricle or from one of its lateral recesses. In six papillomas showing GFA protein in the cells, intracellular fibrils were found in a small number of elongated epithelial cells with the PTAH and/or Masson trichrome stains; in all these six cases, the GFA protein-positive cells were considerably more numerous than cells containing fibrils. Normal choroid plexus epithelium lacks GFA protein, but pathologically altered ependymal cells are often GFA protein-positive. Our findings therefore suggest that focal divergent glial (presumably ependymal) differentiation may be expressed in neoplastic choroid plexus epithelium, consistent with the origin of this epithelium from primitive neuroepithelial (ventricular) cells.This work was supported in part by Research Grant CA-11689 from the National Cancer Institute, USPHS     

Phorbol ester induced changes in tight and adherens junctions in the choroid plexus epithelium and in the ependyma

The molecular composition and functional properties of cell-cell junctions of choroid plexus epithelial cells and the ependyma of the lateral ventricular wall were investigated in the rat brain. Expression studies of cadherin and alpha- and beta-catenins, as well as expression of occludin and ZO-1, indicated that cell adherens and tight junctions were present in both choroid plexus epithelial cells and in ependymal cells. We then tested the hypothesis that phorbolester in vivo can induce changes in the expression level of adherens and tight junction molecules at the blood-cerebrospinal fluid (CSF) barrier as well as in the ependyma. In addition, the functional properties of the ependymal junctions were tested by injection of dextran 3000 into the striatum after phorbolester application. Twenty-four hours after phorbolester-injection into the lateral ventricle of the rat brain, the expression patterns of tight and adherens junction molecules were markedly changed in the epithelial cells of the choroid plexus. The adherens junction proteins cadherin and beta-catenin were reduced in both the ependymal cells of the lateral ventricle and choroid plexus epithelial cells. In addition, the occludin-immunoreactivity of the choroid plexus epithelial cells was strongly reduced. However, the ZO-1 immunoreactivity was not affected by the phorbol ester-treatment and the alpha-catenin immunoreactivity was not changed. Furthermore, phorbol ester injection induced a reduction of the volume of intrastriatal injected biotinylated dextran (m.w. 3000), which is consistent with a modulatory influence of protein kinase C activation on the clearance capacity of the brain.     

Differential expression of cell adhesion molecules (CAM), neural CAM and epithelial cadherin in ependymomas and choroid plexus tumors

A series of frozen specimens of 18 ependymomas and 7 choroid plexus tumors were examined for their expression of cell adhesion molecules, such as neural cell adhesion molecule (NCAM), its polysialylated isoforms (PSA NCAM), and epithelial (E-) cadherin, and of intermediate filament proteins, such as glial fibrillary acidic protein (GFAP) and cytokeratin, using various monoclonal and polyclonal antibodies. Normal choroid plexus and ependyma were taken as controls. Anti-E-cadherin immunoreactivity was observed on the basolateral part of most adult choroid plexus and benign choroid plexus papilloma cells. However, a small number of atypical papillomas and carcinoma cells showed anti- E-cadherin immunoreactivity throughout their cell surface membrane. NCAM were not expressed by adult choroid plexus and benign papilloma cells. Only a few cells expressed NCAM and PSA NCAM in developing choroid plexus, atypical papillomas and carcinomas. Cytokeratin expression was always observed in choroid plexus and their tumors; GFAP expression was variable from case to case. In contrast, ependymal cells and their tumors never expressed E-cadherin but strongly expressed NCAM. PSA NCAM was found in ependymomas exhibiting anaplastic features. All ependymomas strongly expressed GFAP and a few demonstrated slight expression of cytokeratin. These data suggest that, besides GFAP and cytokeratin, NCAM and E-cadherin are of potential diagnostic value in distinguishing choroid plexus tumors from ependymomas. E-cadherin and NCAM may play a role in the functional organization of normal choroid plexus and ependyma, respectively. In particular, incomplete or irregular anti-E-cadherin expression in choroid plexus tumors and PSA NCAM immunoreativity in ependymomas and choroid plexus tumors correlates with the emergence of anaplastic histological features.     

The cerebral ventricles of the dog

Summary The present investigation examined the ependymal linings of the chroid plexus and cerebral ventricles of the dog following a single intracisternal injection of viable, bacillus Calmette-Guerin (BCG). One or 3 days following the injection of BCG, animals were perfused with buffered aldehydes. The choroid plexus of each cerebral ventricle as well as samples of the ependyma from the caudate nucleus, interthalamic adhesion, and median sulcus were removed and prepared for transmission electron microscopy. Following injection of BCG, leukocytic cells are found in assoeiation with the following structures and areas of the subependyma and choroid plexus: the endothelium of small blood vessels and capillaries; the walls of small blood vessels; the subependymal neuropil; the choroid plexus stroma; the single layer of ependyma bordering the luminal surfaces of the choroid plexi and ventricles; and the free, luminal surfaces of the choroid plexus and ventricular ependyma. The population of leukocytic cells included monocytes, macrophages, neutrophils, lymphoblasts, and plasma cells. The results of the present study suggest that the supraependymal leukocyte population of infected animals reaches the cerebral ventricular linings by migrating from the choroidal and subependymal vasculature.Portions of this study were performed in the Department of Anatomy at the University of North Dakota and was supported by the United States Public Health Service Grants NS 09363 and NS 12106, from the Institute of Neurological and Communicative Disorders and Stroke     

Immunohistochemical evidence of endothelin-1 in human choroid plexus

Summary An immunohistochemical investigation was carried out on 17 specimens of human choroid plexus obtained post mortem, 1 biopsy of normal choroid plexus including part of the lateral ventricle and 1 papilloma of the choroid plexus removed surgically. The material was fixed in formalin. Paraffin and cryostat sections were used. A polyclonal antiserum to endothelin-1 served as a primary antibody. The avidin-biotin-peroxidase method was applied to demonstrate the immunoreaction. The epithelial cells of the choroid plexuses, the choroid papilloma and most ependymal cells of the lateral ventricle showed a distinct brown reaction product in their cytoplasm indicating antigenic sites to endothelin-1. The reaction was of lesser intensity in the ependymal cells. The connective tissue in choroid plexus was unstained. A positive immunoreaction was present in the walls of some vessels in the choroid plexus in cryostat sections. This is the first report on the presence of antigenic sites to endothelin-1 in the epithelial cells of the human choroid plexus. The role of endothelin in these cells should be investigated to ascertain if the cells synthesize this biologically active peptide or if it is merely bound to receptors in them.Supported by grants from Swedish Medical Research Council, project 03020, 1987 Års stiftelse för strokeforskning, Selanders stiftelse, Åhlen-stiftelsen and Stiftelsen Gamla Tjänarinnor, Stockholm Sweden     

Immunohistochemical localization of superoxide dismutase in congenital hydrocephalic rat brain

The effects of active oxygen species in the development of congenital hydrocephalus have been investigated. Superoxide dismutase (SOD) is one of the scavengers of active oxygen species and there have been many recent reports on the relationship between neurological disorders by active oxygen species following reperfusion for ischemic brain and SOD. In this study, the localization of Cu-SOD and Zn-SOD in WIC-Hyd congenitally hydrocephalic rat brains was identified by the enzyme unlabeled antibody method. We examined the localization of SOD in the choroid plexus, hippocampus, and ependymal cells of the lateral ventricle and aqueduct of WIC-Hyd rats. SOD was hardly observed in the choroid plexus and faintly localized in the hippocampus and ependymal cells of the congenitally hydrocephalic brain, but was observed equally in the cytoplasm of the choroid plexus, hippocampus, and ependymal cells in control animals. In the hippocampus, less SOD was found in hydrocephalic rats than in controls. The SOD was slightly observed in the CA1 pyramidal cells in hydrocephalic rats. In the lateral ventricle and aqueductal ependyma, less SOD was found in hydrocephalic than in control rats. The amount of Cu, Zn-SOD in the congenitally hydrocephalic rat brain was less than in the control, especially in the choroid plexus. Therefore, we suspect that the production of SOD is congenitally reduced in the congenitally hydrocephalic rat brain, and this may promote the impairment of the function of choroid plexus and cilia due to increased active oxygen species. The reduction of SOD in the choroid plexus, hippocampus and ependymal cells of ventricles or aqueduct may promote the development of hydrocephalus in the congenitally hydrocephalic rat.     

The presence of transthyretin in rat ependymal cells is due to endocytosis and not synthesis

The presence and synthesis of transthyretin, a major carrier protein of thyroxine in rat cerebrospinal fluid, was investigated in choroid plexus epithelial cells and ependymal cells by immunocytochemistry, in situ hybridization, and analysis by Northern and Western blot using a specific oligonucleotide probe and a specific polyclonal antibody to transthyretin. Choroid plexus epithelial cells expressed transthyretin at high levels in developing rat cerebral hemispheres and in cultured cells. These cells secreted transthyretin into the cerebrospinal fluid. In the developing rat brain transthyretin was present in the cytoplasm of ependymal cells, in vesicles in contact with the apical membrane and in cilia. In ependymal cell cultures this protein was particularly abundant in the cilia of these cells. In contrast, ependymal cells did not synthesize transthyretin. It is postulated that transthyretin is transported to ependymal cells from the cerebrospinal fluid by endocytosis.     

Apical localization of the alpha subunit of GTP-binding protein Go in choroidal and ciliated ependymocytes

The presence of GTP-binding proteins (G proteins) has been studied in murine adult choroid plexuses and cultured fetal choroidal or hypothalamic ependymal cells by ADP-ribosylation catalyzed by Bordetella pertussis toxin (PTX) and by immunodetection using affinity-purified polyclonal antibodies against the alpha subunit of the Go protein (Go alpha), the major brain G protein. ADP-ribosylation with 32P-NAD and PTX of choroid plexus revealed an intense labeling at the 40 kDa level in addition to the known PTX-substrates at 41 kDa (Gi alpha) and 39 kDa (Go alpha). This 40 kDa substrate was also predominant in cultured ependymal cells. However, a positive immunoreactivity with the anti-Go alpha antibodies was detected at the level of the 39 kDa faster component, indicating the presence of Go alpha in both choroid plexuses and cultured ependymal cells. In thin frozen sections as well as in cultured cells, Go alpha was mainly immunolocalized at the apical pole of choroidal ependymocytes and in the kinocilia of ciliated ependymal cells. At the ultrastructural level, using gold immunoprobes, the immunoreactivity of a Go alpha-like protein was detected on the cytoplasmic face of the apical plasma membrane, coated pits and vesicles, and in the apical cytoplasmic matrix. In ciliated ependymal cells, the positive immunostaining displayed a dotted pattern at the surface of demembranated axonema of apical kinocilia. These findings strongly suggest that G proteins, especially Go, are involved in transducing chemical signals that modulate traffic and exchanges between cerebrospinal fluid and ependyma through the apical membrane of ependymocytes.     

Neuroblast proliferation on the surface of the adult rat striatal wall after focal ependymal loss by intracerebroventricular injection of neuraminidase

The subventricular zone of the striatal wall of adult rodents is an active neurogenic region for life. Cubic multiciliated ependyma separates the subventricular zone from the cerebrospinal fluid (CSF) and is involved in the control of adult neurogenesis. By injecting neuraminidase from Clostridium perfringens into the right lateral ventricle of the rat, we provoked a partial detachment of the ependyma in the striatal wall. The contralateral ventricle was never affected and was used as the experimental control. Neuraminidase caused widening of the intercellular spaces among some ependymal cells and their subsequent detachment and disintegration in the CSF. Partial ependymal denudation was followed by infiltration of the CSF with macrophages and neutrophils from the local choroid plexus, which ependymal cells never detached after neuraminidase administration. Inflammation extended toward the periventricular parenchyma. The ependymal cells that did not detach and remained in the ventricle wall never proliferated. The lost ependyma was never recovered, and ependymal cells never behaved as neural stem cells. Instead, a scar formed by overlapping astrocytic processes sealed those regions devoid of ependyma. Some ependymal cells at the border of the denudated areas lost contact with the ventricle and became located under the glial layer. Concomitantly with scar formation, some subependymal cells protruded toward the ventricle through the ependymal breaks, proliferated, and formed clusters of rounded ventricular cells that expressed the phenotype of neuroblasts. Ventricular clusters of neuroblasts remained in the ventricle up to 90 days after injection. In the subventricular zone, adult neurogenesis persisted.     

Distribution of epithelial membrane antigen in normal and neoplastic human ependyma

Summary The ependyma and choroid plexus of 23 normal brains and 20 ependymal tumors were examined immunohistochemically for expression of epithelial membrane antigen (EMA) using a specific monoclonal antibody. The ependyma of normal brains showed three patterns of immunoreactivity: membrane immunoreactivity confined to the luminal surface; irregular punctate intracytoplasmic immunore-activity in the subependymal layer; and spherical and ring-like intracytoplasmic immunoreactivity in the subependymal layer. Of 13 differentiated ependymomas 11 reflected the immunoreactive patterns of normal ependyma. The anaplastic ependymomas and ependymoblastomas had no immunoreactivity. Our results indicate that EMA has a highly selective distribution in the ependyma, and is a marker for differentiated ependymoma.     

Interhemispheral neuroepithelial (glio-ependymal) cysts, associated with agenesis of the corpus callosum and neocortical maldevelopment. A case study

Callosal agenesis and interhemispheral cysts containing ependyma, choroid plexus and glial cells are reported in a male infant. To the authors' knowledge this represents the 4th recorded case. Other findings were: nodular neuronal heterotopias with fully differentiated spiny neocortical neurons, widespread neocortical microgyria, cerebellar hypoplasia and bony abnormalities of the foramen magnum and atlas. This study confirms that glio-ependymal cysts are heterotopias of embryonic ventricular epithelium. The existence of more than one type of heterotopia (i.e. neuronal and ependymal) in 1 individual is significant. This indicates an error of cell generation and cell migration affecting the original structure from which both cell types are derived: the embryonic (sub)ventricular zone.     

The involvement of the choroid plexus and ependyma in tuberculosis: its importance in dissemination of the disease in the central nervous system

It is reported in this paper, the study of the choroid plexus and ependyma in 42 cases of tuberculous meningitis. Granulomatous lesions were found as a very frequent lesion in the choroid plexus (75%). In some cases detached granulomas were found free among the villi. The ependymal lesions seen in 97% of the cases are characteristic of the tuberculous granular ependymitis. The report points out the role of these lesions, played in the pathogenesis of the tuberculous meningitis.     

Protein car☐ymethylase activity in the rat superior cervical ganglion during development and after axonal injury

The activity of protein car☐ymethylase (PCM), which catalyzes the transfer of a methyl group from S-adenosyl-l-methionine to car☐yl side chains of proteins to form labile protein-methylesters, was examined in the rat superior cervical ganglion (SCG) and iris during development. In the ganglion the enzyme activity3.3 ± 0.3 (pmol methanol/ganglion/10 min) at birth, gradually increased reaching adult levels28.3 ± 3, by the 30th postnatal day; an 8-fold increase which parallels the increase in protein content. In the iris, one of the target tissues innervated by ganglion neurons, the activity,3.9 ± 0.09 at birth, increases only about 4-fold during development. The source of PCM activity in the iris is mainly in tissues other than sympathetic terminals, since 10 days after removal of the ganglion, about 85% of the enzyme activity is still present in the ipsilateral iris as compared to contralateral controls. One day after crushing the postganglionic nerve, enzyme activity in the proximal nerve stump increases to 126% of control values suggesting an accumulation due to blockade of axonal transport. PCM activity in SCG does not increase after postganglionic nerve section and there is only a transient increase in tyrosine hydroxylase activity. Because the protein content of the ganglion increases after axonal injury, there appear to be decreases in enzyme concentration relative to protein. The results of this study show that during postnatal development protein car☐ymethylase activity in the superior cervical ganglion gradually increases with growth; that the enzyme is present in neurons of the ganglion and may be transported down their axons; and that changes in the enzyme activity during the reaction to axonal injury are comparable to those of other enzymes important in neuronal function.     

A QUANTITATIVE STUDY OF CELL PROLIFERATION IN EPENDYMA AND CHOROID PLEXUS IN THE POSTNATAL RAT BRAIN

Profliferative activity in forebrain ependyma aand choroid plexus epithelium was studied in rats aged up to 42 days by means of autoradiography after injection of [3H]-thymidine. Labelling indices were higher in the lateral than in the third ventricle, while values for choroid plexus epithelium were lower than those for ependyma. In all areas examined, labelling indices showed a similar pattern of decline in the first two postnatal weeks reaching by day 12 a level about 20-30% of that on day 1. This low level, corresponding to a turnover time of 130 days for ependyma, was maintained tereafter up to day 42, indicating the persistence of proliferation in the young adult.     

FGF-2 immunoreactivity in adult rat ependyma and choroid plexus: responses to global forebrain ischemia and intraventricular FGF-2.

Fibroblast growth factor 2 (FGF-2) immunoreactivity (IR) was examined in the ependyma and choroid plexus (CP) of lateral and third ventricles in normal adult rats, as well as in response to transient forebrain ischemia (TFI) and exogenous FGF-2 delivered intraventricularly for several days by osmotic pump. Similar patterns of FGF-2 IR were seen in the CP epithelia of both lateral and third ventricles, as well as in ependymal cells of the third ventricle and along lateral sides of the lateral ventricles. Consistent staining was seen along the apical aspect of epithelial cells facing the cerebrospinal fluid (CSF). Cytoplasmic staining was seen in the absence of ischemia, and was dramatically reduced in response to TFI. FGF-2 treatment followed by TFI resulted in sustained FGF-2 IR within CP and ependymal cells, supporting the idea that these tissues are involved in synthesis and secretion of growth factors into the CSF. In contrast, along the medial sides of the lateral ventricles, adjacent to brain structures such as the hippocampus, consistent staining was seen along the basal aspect of the ependymal cells. We propose that at least some regions of ependyma may function to transport molecules such as FGF-2 directly into the underlying brain parenchyma.     

Differential diagnosis and origin of epithelial cysts in the central nervous system--report of seven cases and review of literature

Seven cases of epithelial cysts are presented with special reference to histological findings. Differential diagnosis and origin of the cysts are also discussed. Two are autopsy cases and 5 are surgical cases. Median age of the patients is 41 years. Three cysts are in the posterior fossa, 1 in the supratentorial region, 1 in both infra- and supratentorial regions and 2 in the spinal canal. On light microscopy, the type of cell lining the cyst wall and the presence of cilia and PAS-positive cells are studied. All cyst walls were lined by a single layer of cuboidal to columnar epithelium. Cilia was seen in 1 and PAS-positive cells were found in 5 out of 7 cases. On electron microscopy of the 4 cases available for study, continuous basement membrane and microvilli were observed in all cases. Coating material covering microvilli was noted in 2 cases. According to these histological findings, these cysts are classified as follows: 1 multiloculated cyst, 1 (respiratory) epithelial cyst, 3 (enterogenous) epithelial cysts, 1 ependymal lined cyst and 1 neuroectodermal cyst. Various non-neoplastic cystic lesions are found in the central nervous system, such as arachnoid cyst, ependymal cyst, colloid cyst, choroid epithelial cyst, neurenteric cyst, and Rathke's cleft cyst. Although histological difference between arachnoid cyst and other epithelium-lined cysts is relatively clear, the precise discrimination between other cystic lesions is difficult and controversial. Some authors have considered these cysts as a neuroectodermal origin because of their histological similarity with choroid plexus or ependyma.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathological alterations of ependyma and choroid plexus after experimental cerebral infection of mice with Sendai virus

Summary The effects of intracerebral inoculation of Sendai virus into young adult mice were investigated by immunofluorescence, light, and electron microscopy. Immunofluorescence of virus-specific antigens was maximal on the third day after inoculation, revealing infection of leptomeninges, ependyma, and choroid plexus. Histologically, meningitis, ependymitis, and choroiditis occurred between the second and third days. The choroiditis was associated with formation of vacuoles within the cytoplasm of epithelial cells. The vacuoles reached diameters up to 50 m. The ubiquitous vacuolization of plexus epithelia resulted in a honeycomb-like pattern. Opaque viral inclusions were visible within the cytoplasm of choroidal and ependymal epithelium as well as in mononuclear inflammatory cells. On electron microscopy, they were composed of intracytoplasmic nucleocapsid accumulations. Viria lay free between microvilli of plexus epithelial cells, and budding virus structures were observed at cellular surfaces. Occasionally, complete viria occurred in the cytoplasm of plexus epithelial cells and were surrounded by a unit membrane from which they appeared to arise by budding. The formation of this small cavity can be interpreted as the first stage of vacuole formation.This investigation was supported by Deutsche ForschungsgemeinschaftSupported by Freie und Hansestadt Hamburg and Bundesministerium für Jugend, Familie und Gesundheit     

Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats.

We tested the hypothesis that populations of ependymal, subependymal and choroid plexus cells proliferate and differentiate after stroke in adult rats. Rats were subjected to 2 h of middle cerebral artery occlusion (n=70) and euthanized at 1, 2, 4, 7, 14, 21 and 28 days (10 per time point). Hematoxylin and eosin staining and immunostaining were performed using antibodies against bromodeoxyuridine, neuronal nuclear antigen and glial fibrillary acidic protein after stroke. In normal nonischemic rats (n=10), single layers of ependymal and choroid plexus cells do not react with bromodeoxyuridine, neuronal nuclear antigen or glial fibrillary acidic protein. Individual subependymal cells express glial fibrillary acidic protein and bromodeoxyuridine, but not neuronal nuclear antigen. After stroke, increased bromodeoxyuridine reactivity was present in multiple layers of ependymal cells and nodules of subependymal cells and in scattered choroid plexus cells from 2 to 28 days and peaked at 7 days. Bromodeoxyuridine immunoreactivity colocalized with neural phenotypes of neuronal nuclear antigen (approximately 0.1-3.5%) and glial fibrillary acidic protein (approximately 8.6%) immunoreactivity in cells in the ventricular zone and the subventricular zone, as well as in the choroid plexus of the ischemia affected hemisphere. Our data suggest that ependymal, subependymal and choroid plexus cells are potential neural precursor cells in the adult mammalian brain.     

Combined neuroepithelial (colloid) cyst and xanthogranuloma (xanthoma) in the third ventricle.

A case is reported of a combined neuroepithelial cyst and xanthogranuloma of the choroid plexus in the third ventricle of a 22-year-old woman. It is suggested that proliferated neuroepithelial cells lining the cyst enter the fibrous wall through the disrupted basal lamina, and then become xanthomatous cells. Disintegration of these foamy epithelial cells releases lipids and other materials into the cyst wall, provoking a response of macrophages and multinucleated giant cells of foreign-body type. A xanthogranuloma is then formed. The origin of "colloid" cysts is from neuroepithelium; these cysts arise from both ependyma and choroid plexus. Those cysts arising in or near the floor of the third ventricle may originate in stomodeal epithelium, but a distinction cannot be made from neuroepithelial cysts by presently available methods.