Developmental Changes of S-100 Protein and Glial Fibrillary Acidic Protein in the Brain in Down Syndrome

Mito, Takashi; Becker, Laurence E.

doi:10.1006/exnr.1993.1052

Cited by 65 publications

(46 citation statements)

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“…Since, apoE is selectively expressed in astrocytes (43), the increase in apoE mRNA in the Ts65Dn mice and in AD may be associated with the activation of astrocytes (hypertrophy) (44). Hypertrophy of astrocytes has been described even in younger DS subjects before gross AD changes have occurred (27,28). There may be similar changes in Ts65Dn mice.…”

Section: Discussionmentioning

confidence: 95%

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Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

Holtzman

Santucci

Kilbridge

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

415

409

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To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse. Ts65Dn mice have an extra copy of the distal aspect of mouse chromosome 16, a segment homologous to human chromosome 21 that contains much of the genetic material responsible for the DS phenotype. Ts65Dn mice show developmental delay during the postnatal period as well as abnormal behaviors in both young and adult animals that may be analogous to mental retardation. Though the Ts65Dn brain is normal on gross examination, there is age-related degeneration of septohippocampal cholinergic neurons and astrocytic hypertrophy, markers of the Alzheimer disease pathology that is present in elderly DS individuals. These findings suggest that Ts65Dn mice may be used to study certain developmental and degenerative abnormalities in the DS brain.

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Section: Discussionmentioning

confidence: 95%

“…Glial abnormalities have been described in both the developing and adult DS brain. These include astrocytic hypertrophy and an increase in astrocyte number (27,28). GFAP is an astrocyte-specific protein.…”

Section: Neurobiology: Holtzman Et Almentioning

confidence: 99%

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

Holtzman

Santucci

Kilbridge

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

415

409

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“…Postnatal developmental changes in S100B were not only found in rats. In the human frontal lobe and hippocampus (CA 1,2,3,4), the number of S100B immunopositive cells increased during early infancy, reached a plateau, and then gradually declined (Mito and Becker 1993). An age-related decrease of S100B and serotonergic fibers was also described in the dentate gyrus of rats, and the authors suggest that the age-related decrease of S100B is responsible for the serotonergic fiber degeneration (Nishimura et al 1995;Frey et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Chronic Fluoxetine Treatment Changes S100B Expression During Postnatal Rat Brain Development

Bock

Koc

Alter

et al. 2013

Journal of Child and Adolescent Psychopharmacology

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Background: Fluoxetine, a selective serotonin reuptake inhibitor, is approved for treatment of childhood depression. In rats, fluoxetine influences neuronal development, but it is unclear whether it also influences glia development. S100B is a gliaderived calcium-binding protein, which may influence the development of serotonergic fibers and, vice versa, serotonin may influence the expression of S100B. Objectives: The purpose of this study was to investigate whether fluoxetine treatment influences the expression of S100B during postnatal development, and whether potential changes are regionally dependent upon the time frame of drug administration. Methods: S100B gene expression and S100B protein expression in three different brain regions (frontal cortex, hippocampus, and striatum) were studied by real-time polymerase chain reaction (PCR) and immunohistochemistry, respectively. First, a short-term effect, 24 hours after a 14 day fluoxetine treatment (5 mg/kg/bw s.c.) of rats either from postnatal day (PD) 1 to 15, 21 to 35, or 50 to 64, was investigated. Then, the same treatment was used to analyze S100B gene and protein levels at PD 90 (long-term effect). Results: At PD 90, a significant increase of gene and protein expression was observed in all regions if rats were treated during PDs 21-35, whereas treatment during other periods had no long-term effects. A short-term effect 24 hours after fluoxetine treatment was found for almost all development stages and regions, demonstrated by a significant increase of S100B. Conclusions: These results support recent research indicating a highly drug-sensitive period (i.e., periadolescence) of rat brain development. Therefore, further clinical studies should be performed to clarify whether such a sensitive period also exists in children.

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“…The gene for S100B is located on human chromosome 21 [7]. The relationship of S100 to human brain disorders is supported by the finding that there is an increase in the level of S100B in the amniotic fluid in trisomy-21 fetuses [8], the number of glial cells expressing S100B is increased in patients with trisomy 21 (Down's syndrome) [9,10] as well as in patients with certain forms of Alzheimer's disease [11,12] associated with similar genetic defects on chromosome 21. Most of the S100 proteins identified on human chromosome 1 have been named using S100A plus a number to identify its location on chromosome 1 (e.g., S100A1, S100A2, etc.).…”

Section: Introductionmentioning

confidence: 62%

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2017

MOJAP

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Using immunohistochemical techniques, the distribution of the "classic" S100 calcium binding proteins, α (A1) and β (B), was determined in the mammalian vestibular end organs. An affinity-purified polyclonal antibody which recognized both the A1 and B subunits and two monoclonal antibodies specific for either the A1 or the B subunit were used in this study. S100A1 was localized specifically to the basal region of the sensory epithelium (saccular macula, cristae ampullaris and utricular macula) when a cross-linking fixative (4% paraformaldehyde) was utilized. Using a fixation protocol including paraformaldehyde and a precipitating fixative revealed an additional localization of S100A1 to the apical region of the saccular macula, cristae ampullaris and utricular macula. This indicates the presence of two populations of S100A1 in these cells: a cytosolic (soluble) component; and a membrane-bound fraction. In contrast, S100B was localized to the layer of the vestibular nerve fibers. Immunoreactivity for S100B was not observed in the sensory epithelium of the saccular or utricular macula or in the cristae ampullaris. The preferential distribution of S100B to the nerve fibers and S100A1 to cells of the sensory epithelium, in two forms (cytosolic and membranebound), may be important in the functional roles of S100 proteins in the vestibular sensory end organs.

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Developmental Changes of S-100 Protein and Glial Fibrillary Acidic Protein in the Brain in Down Syndrome

Cited by 65 publications

References 0 publications

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

Chronic Fluoxetine Treatment Changes S100B Expression During Postnatal Rat Brain Development

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