Reduction of pTau and APP levels in mammalian brain after low-dose radiation
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Abstract Brain radiation can occur from treatment of brain tumors or accidental exposures. Brain radiation has been rarely considered, though, as a possible tool to alter protein levels involved in neurodegenerative disorders. We analyzed possible molecular and neuropathology changes of phosphorylated-Tau (pTau), all-Tau forms, β -tubulin, amyloid precursor protein (APP), glial fibrillary acidic protein (GFAP), ionized calcium binding adaptor molecule 1 (IBA-1), myelin basic protein (MBP), and GAP43 in Frontal Cortex (FC), Hippocampus (H) and Cerebellum (CRB) of swine brains following total-body low-dose radiation (1.79 Gy). Our data show that radiated-animals had lower levels of pTau in FC and H, APP in H and CRB, GAP43 in CRB, and higher level of GFAP in H versus sham-animals. These molecular changes were not accompanied by obvious neurohistological changes, except for astrogliosis in the H. These findings are novel, and might open new perspectives on brain radiation as a potential tool to interfere with the accumulation of specific proteins linked to the pathogenesis of various neurodegenerative disorders.Keywords:
Astrogliosis
Synaptophysin
Gap-43 protein
Astrogliosis
GFAP stain
Clusterin
Gliosis
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Astrogliosis
GFAP stain
Glial scar
Neuroglia
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Astrogliosis
GFAP stain
Gliosis
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Objective To investigate the effect of constraint induced movement therapy( CIMT) on the expression of growth- associated protein 43( GAP- 43) and synaptophysin in cerebral ischemia rats. Methods 90 healthy SD rats were randomly divided into groups sham,model,CIMT,each of 30 cases. Each group was randomly divided into subgroups when 2, 4,8 weeks. Sham group received no treatment,model group and CIMT group received ischemia model. CIMT group received CIMT intervention after 7 days of successful model. The GAP- 43 and synaptophysin mRNA and protein were detected by in situ hybridization and immunohistochemical techniques. Results 2,4 weeks after ischemia model surgery,the GAP- 43 mRNA and protein in CIMT group and model group were higher than those of sham group,CIMT group was higher than those of model group( P 0. 05). 8 weeks after ischemia model surgery,the GAP- 43 mRNA and protein in CIMT group were higher than those of model group and sham group( P 0. 05); the GAP- 43 mRNA and protein between the model group and sham group showed no significant difference( P 0. 05). The synaptophysin mRNA and protein in CIMT group were higher than those of model group and sham group,2,4 weeks after ischemia model surgery,the synaptophysin mRNA and protein in model group were higher than those of sham group( P 0. 05); 8 weeks after ischemia model surgery,the synaptophysin mRNA and protein between model group and sham group showed no significant difference( P 0. 05). Conclusion CIMT can promote the expression of GAP- 43 and synaptophysin and promote synapse occurrence and reconstruction after cerebral ischemia.
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Constraint-induced movement therapy
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The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. Compared with control subjects (CDR = 0), mild (early) AD (CDR = 0.5 to 1) cases had a 25% loss of synaptophysin immunoreactivity. Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins. Thus, synaptic injury in frontal cortex is an early event in AD.
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In Alzheimer's disease (AD), amyloid plaques are surrounded by reactive astrocytes with an increased expression of intermediate filaments including glial fibrillary acidic protein (GFAP). Different GFAP isoforms have been identified that are differentially expressed by specific subpopulations of astrocytes and that impose different properties to the intermediate filament network. We studied transcript levels and protein expression patterns of all known GFAP isoforms in human hippocampal AD tissue at different stages of the disease. Ten different transcripts for GFAP isoforms were detected at different abundancies. Transcript levels of most isoforms increased with AD progression. GFAPδ-immunopositive astrocytes were observed in subgranular zone, hilus, and stratum–lacunosum–moleculare. GFAPδ-positive cells also stained for GFAPα. In AD donors, astrocytes near plaques displayed increased staining of both GFAPα and GFAPδ. The reading-frame–shifted isoform, GFAP+1, staining was confined to a subset of astrocytes with long processes, and their number increased in the course of AD. In conclusion, the various GFAP isoforms show differential transcript levels and are upregulated in a concerted manner in AD. The GFAP+1 isoform defines a unique subset of astrocytes, with numbers increasing with AD progression. These data indicate the need for future exploration of underlying mechanisms concerning the functions of GFAPδ and GFAP+1 isoforms in astrocytes and their possible role in AD pathology.
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Abstract Astrogliosis is a predictable response of astrocytes to various types of injury caused by physical, chemical, and pathological trauma. It is characterized by hyperplasia, hypertrophy, and an increase in immunodetectable glial fibrillary acidic protein (GFAP). As GFAP accumulation is one of the prominent features of astrogliosis, inhibition or delay in GFAP synthesis in damaged and reactive astrocytes might affect astrogliosis and delay scar formation. The aim of this study is to investigate the possibility of utilizing antisense oligonucleotides in controlling the response of astrocytes after mechanically induced injury. We scratched primary astrocyte cultures prepared from newborn rat cerebral cortex with a plastic pipette tip as an injury model and studied the astrogliotic responses in culture. Injured astrocytes became hyperplastic, hypertrophic, and had an increased GFAP content. These observations demonstrate that injured astrocytes in culture are capable of becoming reactive and exhibit gliotic behaviors in culture without neurons. The increase in GFAP content in injured astrocytes could be inhibited by incubating the scratched culture with commerically available liposome complexed with 3′ or 5′ antisense oligonucleotides (20 nt) in the coding region of mouse GFAP. The scratch model provides a simple system to examine in more detail the mechanisms involved in triggering glial reactivity and many of the cellular dynamics associated with scar formation. Antisense oligonucleotide treatment could inhibit the GFAP synthesis in injured astrocytes, hence it may be applicable in modifying scar formation in CNS injury in vivo. © 1993 Wiley‐Liss, Inc.
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GFAP stain
Gliosis
Neuroglia
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To study the effect of melatonin on the expressions of glial fibrillary acidic protein (GFAP), nuclear factor-κB (NF-κB p65) and synaptophysin in mice of different ages.Twenty young male B6C3F1 mice (5.5 months) and 20 aged mice (26 months) were both divided into control and melatonin treatment (daily dose of 0.04 mg/kg) groups. After 2.5 months of treatment, the brain tissues of the mice were collected to examine the expressions of GFAP, NF-κB and SYN by immunohistochemistry.In the control groups, the expression of NF-κB p65 in the brain tissue increased with age, whereas a reverse change was found in melatonin-treated aged rats (P<0.05). Synaptophysin expression also decreased with age, but melatonin treatment significantly enhanced its expression in aged mice (P<0.05). GFAP expression in the brain tissue increased with age regardless of melatonin treatment (P>0.05).GFAP expression is almost not affected by melatonin treatment in aged mice. Melatonin can reduce the expression levels of NF-κB p65 and synaptophysin in the brain tissue to protect the brain and slow down the aging process.
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Astrogliosis
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GFAP stain
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Astrogliosis
GFAP stain
Neuroglia
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