Linked Life Data

18023319

Source:http://linkedlifedata.com/resource/pubmed/id/18023319

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-12-7
pubmed:abstractText
The recent discovery that cellular proliferation was reduced in aneuploid haploid yeast supports a long-standing argument that the developmental neurophenotype of Down syndrome is not uniquely a result of the effects of increased gene dosage. Instead, some phenotypic outcomes appear to resemble those caused by disrupted cellular homeostasis induced by aneuploidy. Decreased cellular proliferation has been identified in the cerebellum and hippocampus of Down syndrome mouse models and in the post-mortem hippocampus and germinal matrix of Down syndrome fetuses. Consistent with predominantly stochastic gene expression and increased energy demands induced by aneuploidy, the "buffering" canalization processes in Down syndrome would be reduced thereby giving rise to increased variance to less stable developmental pathways such as proliferation. The nature and extent of phenotypes due to reduced canalization would depend on the tissue; which is also a question for future research to address. A conceptual model is presented here to demonstrate the nature of influences affecting phenotypes. Ultimately, in Down syndrome, exigent periods of neurodevelopment increasingly appear to reflect the burden of disrupted homeostasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0736-5748
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
539-43
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
A yeast model of Down syndrome.
pubmed:affiliation
The Queensland Brain Institute, The University of Queensland, St. Lucia, Queensland 4072, Australia. r.moldrich@uq.edu.au
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't