Linked Life Data

19110430

Source:http://linkedlifedata.com/resource/pubmed/id/19110430

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-1-13
pubmed:abstractText
Memory deficits in aging affect millions of people and are often disturbing to those concerned. Dissection of the molecular control of learning and memory is paramount to understand and possibly enhance cognitive functions. Old-age memory loss also has been recently linked to altered Ca(2+) homeostasis. We have previously identified DREAM (downstream regulatory element antagonistic modulator), a member of the neuronal Ca(2+) sensor superfamily of EF-hand proteins, with specific roles in different cell compartments. In the nucleus, DREAM is a Ca(2+)-dependent transcriptional repressor, binding to specific DNA signatures, or interacting with nucleoproteins regulating their transcriptional properties. Also, we and others have shown that dream mutant (dream(-/-)) mice exhibit marked analgesia. Here we report that dream(-/-) mice exhibit markedly enhanced learning and synaptic plasticity related to improved cognition. Mechanistically, DREAM functions as a negative regulator of the key memory factor CREB in a Ca(2+)-dependent manner, and loss of DREAM facilitates CREB-dependent transcription during learning. Intriguingly, 18-month-old dream(-/-) mice display learning and memory capacities similar to young mice. Moreover, loss of DREAM protects from brain degeneration in aging. These data identify the Ca(2+)-regulated "pain gene" DREAM as a novel key regulator of memory and brain aging.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0445
pubmed:author
pubmed:issnType
Electronic
pubmed:day
13
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-60
pubmed:dateRevised
2010-1-17
pubmed:meshHeading
pubmed-meshheading:19110430-Aging, pubmed-meshheading:19110430-Analysis of Variance, pubmed-meshheading:19110430-Animals, pubmed-meshheading:19110430-Blotting, Western, pubmed-meshheading:19110430-Calcium, pubmed-meshheading:19110430-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:19110430-DNA, pubmed-meshheading:19110430-DNA Primers, pubmed-meshheading:19110430-Electrophoretic Mobility Shift Assay, pubmed-meshheading:19110430-Electrophysiology, pubmed-meshheading:19110430-Hippocampus, pubmed-meshheading:19110430-Immunohistochemistry, pubmed-meshheading:19110430-Kv Channel-Interacting Proteins, pubmed-meshheading:19110430-Learning, pubmed-meshheading:19110430-Memory, pubmed-meshheading:19110430-Mice, pubmed-meshheading:19110430-Mice, Knockout, pubmed-meshheading:19110430-Repressor Proteins, pubmed-meshheading:19110430-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2009
pubmed:articleTitle
Lack of DREAM protein enhances learning and memory and slows brain aging.
pubmed:affiliation
División de Neurociencias, Universidad Pablo de Olavide de Sevilla, Carretera de Utrera Km. 1, 41013-Sevilla, Spain.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't