Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific combination of homeobox genes is proposed to be decisive in the terminal differentiation of neuronal systems. In order to identify combined expression of homeobox genes in the ventral forebrain, a reverse transcriptase-polymerase chain reaction strategy using degenerated primers was employed. We identified, amongst others, Lhx7 and Gbx1, displaying a marked overlapping expression in septal and pallidal areas. Gbx1 and Lhx7 were both expressed in those adult brain nuclei that collectively form the basal forebrain cholinergic system, a prime target of neurodegeneration in Alzheimer's disease. Indeed, we detected Lhx7 within cholinergic neurons, whereas the related Lhx6 gene was found in adjacent neurons. From these data we suggest that combined expression of Lhx7 and Gbx1 plays a role in the development of the cholinergic system of the basal forebrain. It is speculated that both genes remain participating in molecular processes in the adult cholinergic neurons, and can be employed to study regulation and survival of these neurons under normal and pathological conditions.
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PMID:The homeobox genes Lhx7 and Gbx1 are expressed in the basal forebrain cholinergic system. 1180 65

One of the pathological hallmarks of Alzheimer's disease (AD) is the presence of amyloid plaques. The main constituent of the amyloid plaques is the amyloid beta-peptide (A beta) shown to activate glial cells in vitro. A growing body of evidence suggests that these cells contribute to neurotoxicity through production of inflammatory cytokines, chemokines, and neurotoxic substances, such as reactive oxygen species (ROS). In this study, mRNA levels of the inflammatory cytokines interleukin (IL)-1alpha and beta, and IL-6 were analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) in rat primary mixed glial cells after treatment with A beta(25-35), a biologically active fragment of A beta peptide with neurotoxic properties. Clear morphological changes of the astrocytes, as well as proliferation and clustering of microglial cells were observed by light and immunofluorescence microscopy after 24 h treatment. Significant increases in IL-1alpha and IL-6 mRNA levels were detected after 24 and 72 h, whereas significantly increased levels of IL-1beta mRNA could only be detected after 4 h treatment. The most pronounced effect was seen on IL-6 mRNA expression, which increased approx two- to threefold after treatment. In addition, increased secretion of IL-6 was detected after 96 h exposure. Recently, association of IL-1alpha and IL-6 gene polymorphism with AD was reported, suggesting that these cytokines may play an important role in the development of the disease. The increased mRNA levels of IL-1alpha and IL-6 in parallel with the morphological changes in the mixed glial-cell cultures support that these cytokines may be involved in A beta-induced gliosis and in the pathogenesis of AD.
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PMID:Increased gene expression of interleukin-1alpha and interleukin-6 in rat primary glial cells induced by beta-amyloid fragment. 1185 30

Metal ions play an important role in health and disease by influencing cellular biochemical pathways. The increased concentrations of some metal ions may have cytotoxic effects through their ability to oxidatively modify biomolecules, which may cause oxidative stress-induced brain cell death leading to neurodegenerative disorders observed in Alzheimer's disease (AD). We therefore performed elemental analysis of human brain tissues by a sophisticated method of inductively coupled plasma mass spectrometry (ICP-MS) in two regions of the AD brain, the parietal cortex and cerebellum, and compared them with the age-matched control. Our analysis shows the differential distribution of some metal ions in the two regions of the brain. Most importantly, Si, Sn, Al and Mn showed significantly higher levels in the parietal cortex of the AD brain compared to the control. The other metal ions showing moderate increases in the parietal cortex were Na, Te, Cr, Fe and B. Since these metal ions can modify lipoproteins in the brain and modified lipoproteins are taken up by scavenger receptors class B type I (SR-BI), we also determined the presence of SR-BI in the parietal cortex and cerebellum regions of the control and AD brains using a sensitive method, the reverse transcriptase-polymerase chain reaction. Our results suggest that SR-BI are present in the parietal cortex as well as in the cerebellum of the control and AD brains, suggesting that the presence of SR-BI may be involved in the uptake of oxidatively modified lipoproteins and beta-amyloid (Abeta) protein complexed with apoE, suggesting implications in the progression of late onset AD and other neurodegenerative disorders characterized by the deposition of insoluble aggregates observed in the AD brain.
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PMID:Scavenger receptor class B type I expression and elemental analysis in cerebellum and parietal cortex regions of the Alzheimer's disease brain. 1195 56

The N-methyl-D-aspartate (NMDA) receptor is a subtype of ionotropic glutamate receptor that is involved in synaptic mechanisms of learning and memory, and mediates excitotoxic neuronal injury. In this study, we tested the hypothesis that NMDA receptor subunit gene expression is altered in Alzheimer's disease (AD), especially in brain regions known to be important in memory. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the messenger RNA (mRNA) levels of the NMDA receptor subunits NR1, NR2A, and NR2B in the hippocampus and entorhinal cortex of postmortem brain samples from nine clinically well-characterized AD patients and nine aged controls. Cerebellum, a site minimally affected by AD, was also chosen for comparison assessment. Results showed decreased levels of the NR2 mRNAs in AD brains compared to controls. Reductions of NR2A (46.2%, p<0.01) and NR2B (43.2%, p<0.0001) mRNA levels were identified in the entorhinal cortex. Reductions of NR2A (41.4%, p<0.05) and NR2B (40.6%, p=0.058) mRNA levels were found in the hippocampus. NR1 mRNA levels were similar in all three brain regions in both AD and controls. No significant changes of subunit NR2A and NR2B mRNA levels were identified in the cerebellum. Postmortem delay (PMD), tissue storage time, brain weight, or age of the subjects did not affect these changes. These data suggest that alterations in NMDA receptor subunits, especially the NR2A and NR2B, may be important in AD, particularly in neuronal populations that underlie impaired learning and memory.
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PMID:N-methyl-D-aspartate receptor subunit NR2A and NR2B messenger RNA levels are altered in the hippocampus and entorhinal cortex in Alzheimer's disease. 1212 70

The main constituent of the Alzheimer amyloid plaques is the amyloid beta (Abeta) peptide shown to activate glial cells in vitro. Activated glial cells are believed to contribute to neurotoxicity through production of inflammatory cytokines, such as interleukin-1 (IL-1), chemokines and neurotoxic substances. The IL-1 system has been proposed to play a role in neurodegenerative processes and can in turn induce expression of other cytokines such as IL-6. Recently, association of IL-1 and IL-6 gene polymorphism with Alzheimer's disease was reported, suggesting that these cytokines may play an important role in the development of the disease. In this study, rat primary mixed glial cells were treated with IL-1beta, Abeta(1-42) or Abeta(25-35). As expected the different treatments all resulted in activation of the transcription factor NFkappaB observed by electrophoretic mobility shift assay. Significant increases in IL-1beta and IL-6 mRNA levels, as analysed by reverse transcriptase-polymerase chain reaction (RT-PCR), were detected after the different treatments. In addition, increased secretion of IL-6 was detected by ELISA after 96 h exposure in response to IL-1beta, Abeta(1-42) or Abeta(25-35). When cells were exposed to both IL-1beta and Abeta(25-35) additive effects were observed. This supports that the effect of Abeta can be potentiated by concurrent exposure to inflammatory cytokines and that the IL-1 system is not necessary for Abeta effects on IL-6 expression in agreement with previous studies.
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PMID:Additive effects of amyloid beta fragment and interleukin-1beta on interleukin-6 secretion in rat primary glial cultures. 1216 95

The brain is a heterogeneous tissue in which the numbers of neurons, glia, and other cell types vary among anatomic regions. Gene expression studies performed on brain homogenates yield results reflecting mRNA abundance in a mixture of cell types. Therefore, a method for quantifying gene expression in individual cell populations would be useful. Laser capture microdissection (LCM) is a new technique for obtaining pure populations of cells from heterogeneous tissues. Most studies thus far have used LCM to detect DNA sequences. We developed a method to quantify gene expression in hippocampal neurons from mouse brain using LCM and real-time reverse transcriptase-polymerase chain reaction (RT-PCR). This method was optimized to permit histochemical or immunocytochemical visualization of nerve cells during LCM while minimizing RNA degradation. As an example, gene expression was quantified in hippocampal neurons from the Tg2576 mouse model for Alzheimer's disease.
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PMID:Analysis of neuronal gene expression with laser capture microdissection. 1221 Aug 23

Previous studies have suggested the involvement of amyloid precursor protein (APP) in Alzheimer's disease (AD), as exons 16 and 17 of the APP gene mutations have been found in some familial AD patients. Furthermore, overexpression and deposition of the beta amyloid peptide, a proteolytic product of APP, have been considered as a pathological hallmark of Alzheimer's disease. Therefore, it is of particular interest to determine the expression of APP gene at the transcription level for better understanding of the roles of APP gene in AD pathogenesis. In this work, we employed the quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to quantify APP mRNA transcripts in the peripheral mononuclear blood cells (PMBC) of 52 Alzheimer's patients, 28 vascular dementia (VD) patients, and 60 healthy elderly controls. The results showed that the amount (mean +/- SEM) of APP transcripts per microgram of total cDNA was 4.05 +/- 0.27, 2.73 +/- 0.33, and 2.59 +/- 0.27 amole in AD, VD, and healthy controls, respectively. There was a significant increase (P < 0.05) in the expression of APP mRNA transcripts in AD compared with that in VD or in healthy controls. Thus, our data indicated that variation of APP gene expression in PMBC might be a pathogenic source of Alzheimer's disease.
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PMID:Enhanced production of amyloid precursor protein mRNA by peripheral mononuclear blood cell in Alzheimer's disease. 1262 74

In cases of traumatic brain injury (TBI) in which the patient survived for only a short period of time and was without macroscopic changes at autopsy, it is difficult to diagnose TBI. To detect early diagnostic markers of diffuse axonal injury (DAI), real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) in an experimental head trauma model of rat was chosen. The beta-amyloid precursor protein (beta-APP) is a well-known diagnostic marker of DAI which can be detected by immunolabeling as early as 1.5 h after injury. beta-APP has a binding protein, FE65, which is expressed in the brain of Alzheimer's disease patients along with beta-APP, but no involvement with brain injury has been reported. Neuron-specific enolase (NSE) is also a useful marker of DAI. We found that FE65 expression increased dramatically as early as 30 min after injury and decreased after peaking 1 h post-injury, although NSE showed no significant changes. These results suggest that real-time PCR of FE65 mRNA is useful for the diagnosis of DAI in forensic cases.
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PMID:Real-time PCR quantitation of FE65 a beta-amyloid precursor protein-binding protein after traumatic brain injury in rats. 1270 77

Previous studies suggest that female sex hormones modulate synaptic zinc levels, which may influence amyloid plaque formation and Alzheimer's disease progression. We examined the effects of ovariectomy and estrogen supplement on the levels of synaptic zinc and zinc transporter protein Znt3 in the brain. Ovariectomy was performed on 5-month-old mice, and 2 weeks later, pellets containing vehicle, low (0.18 mg/pellet), or high dose (0.72 mg) 17beta-estradiol were implanted. After 4 weeks, animals were decapitated, and blood and brain were collected for analysis. Blood analysis indicated that estrogen implants altered plasma estrogen levels in a dose-dependent manner. Analysis of brain tissue showed that ovariectomy raised hippocampal synaptic vesicle zinc levels, whereas estrogen replacement lowered these zinc levels. Western blots revealed that Znt3 levels in the brain were modulated in parallel with synaptic zinc levels, whereas no change was detected in the levels of Znt3 mRNA, as determined by Northern blot and reverse transcriptase-PCR analysis. However, mRNA levels of the delta subunit of adaptor protein complex (AP)-3, which modulates the level of Znt3 levels, were altered by estrogen depletion or replacement. These data demonstrate that estrogen alters the levels of Znt3 and synaptic vesicle zinc in female mice, probably through changing AP-3 delta expression. Since synaptic zinc may play a key role in neuronal death in acute brain injury as well as in plaque formation in Alzheimer's disease, and since estrogen may be beneficial in both conditions, our results may provide new insights into the effects of estrogen on the brain.
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PMID:Estrogen decreases zinc transporter 3 expression and synaptic vesicle zinc levels in mouse brain. 1468 Dec 34

It has been considered that tumor necrosis factor alpha (TNFalpha) is participated in the Alzheimer's, and Parkinson's diseases, brain injury and brain ischemia. However, expression of TNFalpha after brain ischemia has not been demonstrated in detail. Therefore we examined the cellular expression of TNFalpha during and after transient middle cerebral artery occlusion (tMCAO) in mice by use of reverse transcriptase-polymerase chain reaction and immunohistochemical technique. TNFalpha mRNA expression was gradually increased in the neocortex of the ipsilateral hemisphere during ischemia and peaked at 1 hour after reperfusion. Then, the mRNA expression decreased and peaked again at 24 hours after reperfusion. TNFalpha-like immunoreactivities were observed in the process such as dendrite of neuron slightly before ischemia, and markedly increased in neurons in addition to the process of the ipsilateral hemisphere at 1 and 24 hours after ischemia. The results suggest that the expression of TNFalpha is up-regulated in the neurons after tMCAO. TNFalpha may induce ischemic neuronal cell death during ischemic insult.
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PMID:Expression of tumor necrosis factor alpha (TNFalpha) following transient cerebral ischemia. 1475 13


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