Gene expression in fetal Down Syndrome brain as revealed by subtractive hybridization

Labudova, Olga; Kitzmueller, Erwin; Rink, H.; Cairns, Nigel J.; Lübec, Gert

doi:10.1007/978-3-7091-6380-1_8

Cited by 7 publications

(4 citation statements)

References 33 publications

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“…More specifically, TFs for e. g. Fos (see above) and nuclear factor kappa B (NF-kB), [40] deranged in DS brain [45], have been shown to strongly interact with the redox system (Fig. 2).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 97%

The brain in Down syndrome (TRISOMY 21)

Lubec

Engidawork

2002

Journal of Neurology

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Down syndrome (DS) is the most common genetic birth defect associated with mental retardation. The mechanism(s) underlying the neuropathology of DS is not completely understood. Different hypotheses have been advanced to explain this mystery, including the gene dosage effect, the amplified developmental instability, and the molecular misreading concept. Overexpression of genes residing in chromosome 21 has been assumed to be a central point in the neuropathology of DS, although reports disagreeing with this notion have also been published. In addition, an accumulating body of evidence indicates that genes located on other chromosomes are also involved in the process. DS thus appears to be a disease process involving numerous gene products and this interaction and interplay in the final analysis determines the outcome of the disease. In this regard, transcription factors, reactive oxygen species and apoptosis related proteins are viewed as potential candidates that play a significant role in the disease process. Therapeutic modalities that target these factors including antioxidants and caspase inhibitors might have some benefit in alleviating the symptoms of DS.

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“…More specifically, TFs for e. g. Fos (see above) and nuclear factor kappa B (NF-kB), [40] deranged in DS brain [45], have been shown to strongly interact with the redox system (Fig. 2).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 97%

The brain in Down syndrome (TRISOMY 21)

Lubec

Engidawork

2002

Journal of Neurology

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“…The principles underlie the “gene hunting”-technology of “subtractive hybridisation”, applied to profile differentially expressed gene-transcripts, has been described in several publications [ 33 – 35 ].…”

Section: Expression Profiling By “Gene Hunting”- Technology Discoverementioning

confidence: 99%

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

et al. 2011

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Perinatal Asphyxia—oxygen deficit at delivery—can lead to severe hypoxic ischaemic organ damage in newborns followed by a fatal outcome or severe life-long pathologies. The severe insults often cause neurodegenerative diseases, mental retardation and epilepsies. The mild insults lead to so-called “minimal brain-damage disorders” such as attention deficits and hyperactivity, but can also be associated with the development of schizophrenia and life-long functional psychotic syndromes. Asphyxia followed by re-oxygenation can potentially lead to development of several neurodegenerative pathologies, diabetes type 2 and cancer. The task of individual prediction, targeted prevention and personalised treatments before a manifestation of the life-long chronic pathologies usually developed by newborns with asphyxic deficits, should be given the extraordinary priority in neonatology and paediatrics. Socio-economical impacts of educational measures and advanced strategies in development of robust diagnostic approaches targeted at effected molecular pathways, biomarker-candidates and potential drug-targets for tailored treatments are reviewed in the paper.

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“…1999). On the other hand, scleraxis, a basic helix–loop–helix type transcription factor that regulates growth and differentiation of numerous cells, is up‐regulated (Labudova et al . 1999).…”

Section: Transcription and Translation Machinerymentioning

confidence: 99%

“…Alternatively, it is possible that different subtypes of transcription factors differentially regulate gene expression. Not unlike REST, the junD component of the AP-1 transcription factors implicated in neurogenesis and nuclear factor-kappa B, a transcriptional regulator of a multitude of genes involved in immune and inflammatory responses, is decreased in fetal DS brain (Labudova et al 1999). On the other hand, scleraxis, a basic helix-loop-helix type transcription factor that regulates growth and differentiation of numerous cells, is up-regulated (Labudova et al 1999).…”

Section: Transcription and Translation Machinerymentioning

confidence: 99%

Molecular changes in fetal Down syndrome brain

Engidawork

Lubec

2003

Journal of Neurochemistry

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Trisomy of human chromosome 21 is a major cause of mental retardation and other phenotypic abnormalities collectively known as Down syndrome. Down syndrome is associated with developmental failure followed by processes of neurodegeneration that are known to supervene later in life. Despite a widespread interest in Down syndrome, the cause of developmental failure is unclear. The brain of a child with Down syndrome develops differently from that of a normal one, although characteristic morphological differences have not been noted in prenatal life. On the other hand, a review of the existing literature indicates that there are a series of biochemical alterations occurring in fetal Down syndrome brain that could serve as substrate for morphological changes. We propose that these biochemical alterations represent and/or precede morphological changes. This review attempts to dissect these molecular changes and to explain how they may lead to mental retardation.

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Gene expression in fetal Down Syndrome brain as revealed by subtractive hybridization

Cited by 7 publications

References 33 publications

The brain in Down syndrome (TRISOMY 21)

The brain in Down syndrome (TRISOMY 21)

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

Molecular changes in fetal Down syndrome brain

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