R. Ferrando-Miguel, K. Shim, M. Cheon, M. Gimona, M. Furuse, G. Lubec
{"title":"Overexpression of Interferon α/β Receptor β Chain in Fetal Down Syndrome Brain","authors":"R. Ferrando-Miguel, K. Shim, M. Cheon, M. Gimona, M. Furuse, G. Lubec","doi":"10.1159/000079401","DOIUrl":"https://doi.org/10.1159/000079401","url":null,"abstract":"Background: Down syndrome (DS; trisomy 21) is the most common chromosomal aberration, with an incidence of 1/700 live births, and presents with mental retardation, typical phenotype and a series of associated pathological conditions. Although overexpression of genes encoded on chromosome 21 was proposed to lead to the phenotype, this has not been fully addressed at the protein level. Aim: It was therefore the aim of our study to determine protein levels of several chromosome 21 gene products in fetal DS brain. We selected interferon (IFN) α/β receptor β chain (IFNAR2), glutamate receptor 5 (ionotropic kainate 1), h2 calponin, claudin-8 and oligodendrocyte transcription factor 1 for quantification in fetal brain of the early second trimester using immunoblotting. Results: We observed significant and about twofold overexpression of the 20-kD immunoreactive IFN receptor α/β band in the fetal cortex of DS brain (p = 0.0293), while the 70-kD immunoreactive band was overexpressed but did not reach statistical significance (p = 0.065). When data were normalized to the housekeeping protein β-actin, a significant increase in IFN receptor levels was observed. Levels of the aforementioned proteins were comparable between DS and controls. Conclusion: Overexpression of IFNAR2 in fetal DS brain may increase the responsiveness of DS cells, leading to altered neuronal excitability, neuronal growth and survival as well as cytoskeleton derangement.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"2 1","pages":"147 - 155"},"PeriodicalIF":0.0,"publicationDate":"2004-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000079401","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65234547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Molecular Synaptosomal Deficit in Down Syndrome Starts Early in Life","authors":"D. Pollak, M. Fountoulakis, G. Lubec","doi":"10.1159/000079400","DOIUrl":"https://doi.org/10.1159/000079400","url":null,"abstract":"Information about brain abnormalities in early prenatal life leading to or representing mental retardation in Down syndrome (DS) is limited. Synaptic dysgenesis was described and is considered the morphological correlate of mental retardation. The availability of appropriate fetal brain samples along with the advent of proteomic technologies unambiguously identifying proteins concomitantly made us study synaptosomal structures at the molecular level in the fetal cortex of controls and DS fetuses. Cortical tissue of seven controls (mean 18.8 weeks of gestation) and eight DS fetuses (mean 19.8 weeks of gestation) was homogenized, proteins were extracted and run on two-dimensional gel electrophoresis followed by mass spectrometrical analysis using MALDI-TOF (matrix-assisted laser desorption ionization – time of flight). Levels of synaptic proteins N-ethylmaleimide-sensitive fusion protein (controls: mean 0.030 ± 0.015; DS: mean 0.011 ± 0.008 O.D.), synaptotagmin I (controls: mean 0.038 ± 0.021; DS: mean 0.010 ± 0.002 O.D.) and septin 3 (controls: mean 0.061 ± 0.002; DS: mean 0.019 ± 0.012 O.D.) were significantly decreased in brains of fetuses with DS. It is concluded that an altered expression of synaptosomal proteins at the time of the early second trimester of gestation may form the structural basis for the brain deficit in DS early in life.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"2 1","pages":"143 - 146"},"PeriodicalIF":0.0,"publicationDate":"2004-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000079400","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65234484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Genetic, Environmental and Immunologic Factors in the Etiology of Autism Spectrum Disorders","authors":"S. Bölte, F. Poustka","doi":"10.1159/000079404","DOIUrl":"https://doi.org/10.1159/000079404","url":null,"abstract":"Autism spectrum disorders are early-onset chronic conditions of qualitatively impaired social interaction and reciprocal communication with an estimated prevalence rate of 0.6%. Autism is heterogeneous in phenotype and comorbidity. Its precise etiology remains largely an enigma, but twin and family studies indicate substantial hereditary fundamentals. In this report, we briefly review the progress of molecular genetic, environmental and (auto-)immunologic research in autism and similar conditions. At the present time, idiopathic autism is assumed to be an oligogenic epistatic disorder. In a minority of cases, some Mendelian syndromes and other medical conditions as well as exogenous and immune mechanisms may also cause or trigger autism. A standard epidemiologic vulnerability model has been proposed to integrate possible major and minor risks of different origin.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"2 1","pages":"175 - 179"},"PeriodicalIF":0.0,"publicationDate":"2004-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000079404","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65234886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Ferrando-Miguel, S. Bölte, F. Poustka, M. Cheon, W. Y. Tam, Fung Yip, W. Chan, M. Gimona, H. Yeung, Daniel Kwong On Chan, Chris K.C. Wong, D. Pollak, M. Fountoulakis, Gert Lubec, K. Shim, M. Furuse, C. S. Cheung, Liang Wang, M. Dong
{"title":"Subject Index Vol. 4, 2003","authors":"R. Ferrando-Miguel, S. Bölte, F. Poustka, M. Cheon, W. Y. Tam, Fung Yip, W. Chan, M. Gimona, H. Yeung, Daniel Kwong On Chan, Chris K.C. Wong, D. Pollak, M. Fountoulakis, Gert Lubec, K. Shim, M. Furuse, C. S. Cheung, Liang Wang, M. Dong","doi":"10.1159/000080724","DOIUrl":"https://doi.org/10.1159/000080724","url":null,"abstract":"","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"2 1","pages":"190 - 190"},"PeriodicalIF":0.0,"publicationDate":"2004-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000080724","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65244986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Migration of Hindbrain Neural Crest Cells in the Mouse","authors":"C. S. Cheung, Liang Wang, M. Dong, W. Chan","doi":"10.1159/000079403","DOIUrl":"https://doi.org/10.1159/000079403","url":null,"abstract":"Background: Neural crest cells are a special group of embryonic cells which are able to emigrate from the dorsal neural tube (the developing central nervous system) to the mesenchyme and form different derivatives in embryos. In contrast to the situation in the avian embryo, where the use of quail-chick chimeras has provided much information on neural crest migration, the early migratory pathways of hindbrain neural crest cells are not well understood in mammals. Aims: In the present study, an exogenous dye, wheat germ agglutinin-gold conjugate (WGA-Au), was used to label the early migrating hindbrain neural crest cells to track their migration at three axial levels, namely (1) pre-otic, (2) post-otic and pre-somitic, and (3) somitic (somites 1–4) levels, in mouse embryos cultured in vitro. Results: It was found that neural crest cells had already started their emigration from the dorsal part of the neural tube at the 9-somite stage and migrated into the mesenchyme subjacent to the neural tube. When the labelled embryos were cultured to more advanced stages, neural crest cells migrated to more ventral regions. At the 13-somite stage, most neural crest cells at the pre-somitic hindbrain migrated to the mesenchyme lateral to the dorsal aorta, while by the 17-somite stage, labelled cells reached the mesenchyme adjacent to the pharynx, which is located more ventrally than the dorsal aorta. At the 21-somite stage, more labelled cells were found in the mesenchyme lateral and ventral to the pharynx. At the somitic level, neural crest cells migrated along three distinct routes, namely the dorsolateral (between the surface epithelium and the somite), medial (between the somite and the neural tube) and intersomitic (between two consecutive somites) pathways. Conclusions: Our results indicate that whole embryo culture is able to support the normal development of mouse embryos at early organogenesis in vitro for 26 h, and that WGA-Au is an ideal short-term cell marker for tracking neural crest migration in the mouse. We also show that the migratory patterns of hindbrain neural crest cells in the mouse largely resemble those observed in the chick.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"2 1","pages":"164 - 174"},"PeriodicalIF":0.0,"publicationDate":"2004-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000079403","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65234872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P. Vidal, H. Straka, N. Vibert, L. Moore, C. de Waele
{"title":"Recovery after Vestibular Lesions: From Animal Models to Patients","authors":"P. Vidal, H. Straka, N. Vibert, L. Moore, C. de Waele","doi":"10.1159/000096797","DOIUrl":"https://doi.org/10.1159/000096797","url":null,"abstract":"Gaze and postural stabilization is the result of a complex multisensory integration, which can be defined as the process of matching multiple internal representations of an external event (head and/or trunk rotation), obtained from different sensory modalities, into a unique intrinsic frame of reference in which appropriate motor commands can be coded. Despite the importance of the labyrinths, their lesions are not rare. They result in static and dynamic deficits. What is remarkable is that some of these deficits recover in mammalian species, including humans: the vestibular compensation process refers to the complete or partial normalization of the static and dynamic postural and ocular motor deficits. In the following, only two aspects of vestibular compensation will be discussed: (1) the relationship between the recovery of the vestibulo-ocular reflexes and the postlesional plasticity of the intrinsic membrane properties of the medial vestibular nucleus, and (2) the relationship between the postural recovery and the vestibular control of the skeletal geometry at large. Subsequently, the results of investigations in animal models will be related to some clinical findings. While such an exercise is highly speculative, it points to new directions for clinical research and vestibular rehabilitation.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"15 1","pages":"194 - 206"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000096797","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64366096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thalamocortical and Corticothalamic Interaction in the Auditory System","authors":"Zhuo Zhang, Y. Chan, Jufang He","doi":"10.1159/000096801","DOIUrl":"https://doi.org/10.1159/000096801","url":null,"abstract":"The neuronal interconnections between thalamus and cortex modulate information transmission in the central auditory system. To facilitate the understanding of its modulation effects and mechanism, first, the recent progress on investigating the anatomical connections and the physiological properties of the medial geniculate body and auditory cortex is summarized. Second, the connectional pattern and functional organization in thalamocortical and corticothalamic network are described. Third, the strategic position and role of the thalamic reticular nucleus in the auditory system are demonstrated. Lastly, the functional implication of this integrated system and possible interactions between auditory thalamus and cortex are discussed. The thalamocortical and corticothalamic projections may work as a dynamic filter array in integrating sensory information and optimizing signal processing in the auditory system.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"3 1","pages":"239 - 248"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000096801","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64366548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Plants Beneficial to the Aging Brain","authors":"T. Ng, H. Wang, F. Liu, L.X. Xia","doi":"10.1159/000094576","DOIUrl":"https://doi.org/10.1159/000094576","url":null,"abstract":"A number of edible plants and/or their constituents have been shown to delay the degenerative changes in the brain associated with aging. These plants included Allium sativum, Aloe vera, Astragalus membranaceus, Boschniakia rossica, Clitoria ternatea, Curcuma phaeocaulis, Capsicum annum, Cyanum wildfordii, Emblica officinals, Ginkgo biloba, Heteropteris aphrodisiaca, Panax ginseng, Pegasus laternarius, Polygonum multiflorum, Ptychopetalum olacoides, Scutellaria baicalensis, Valeriane officinalis, Withania somnifera and Zingiber officinale. Among these plants, the best known are G. biloba and P. ginseng.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"3 1","pages":"136 - 141"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000094576","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64345312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yan Shi, Weiyi Yang, Jin-Shan Zhang, T. C. Leung, K. Yung
{"title":"Effects of Traditional Chinese Medicine Radix Astragali, Fructus Aurantii and Rhizoma Cypei Extracts on c-Fos Expression in the Aging Rat Hippocampus Induced by Exercise","authors":"Yan Shi, Weiyi Yang, Jin-Shan Zhang, T. C. Leung, K. Yung","doi":"10.1159/000094555","DOIUrl":"https://doi.org/10.1159/000094555","url":null,"abstract":"Fatigue is a complex interaction between the peripheral systems and the central nervous system and is often a problem in aging individuals. In accordance with the view of traditional Chinese medicine, treatment of fatigue, as induced by heavy exercise, is related to the restoration of Qi in the body. In order to investigate the effects of two formulations of traditional Chinese medicine, namely the Qi-supplementing (QS) medicine containing radix astragaliand the QS formulation plus Qi-rectifying (QR) medicine containing radix astragali, fructus aurantii and rhizoma cypei, which are often used in elderly individuals, aging rats which were exercised for 5 weeks were treated with the above two formulations. Immunocytochemistry revealed that the number of Fos-immunoreactive neurons in the CA1 and CA2 regions of the hippocampus was significantly increased after heavy exercise. Treatment with the QS + QR formulation but not the QS formulation was able to downregulate the number of Fos-immunoreactive neurons in the CA1 and CA2 regions of the hippocampus to the levels of the nonexercise controls. These results indicate that the Chinese medicine formulations, notably the QS + QR formulation, are effective in the restoration of normal levels of Fos protein expression in the central nervous system after heavy exercise. These results have important implications in the treatment of fatigue in aging individuals using formulations of traditional Chinese medicine.","PeriodicalId":89607,"journal":{"name":"Neuroembryology and aging","volume":"3 1","pages":"123 - 127"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000094555","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64345204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}