Linked Life Data

12811583

Source:http://linkedlifedata.com/resource/pubmed/id/12811583

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-9-26
pubmed:abstractText
Alzheimer's disease (AD) is a disorder of brain self organization associated with morphodysregulation at the synaptic level. Disturbances follow a hierarchical spatio-temporal pattern throughout the cortex and involve the re-activation of developmental molecular programs. The large glycoprotein reelin, synthesized by Cajal-Retzius (CR) cells, is an important component of a signaling pathway involved in embryonic development and modulation of synaptic circuitry, but is also implicated in the pathogenetic cascade in AD. Although the majority of CR cells sequentially disappears from the postnatal cortical layer I, a few of them persist in the normal adult brain. They continue to produce reelin, express a variety of other proteins, and are characterized by a typical morphology. Recently, CR cells have been reported to be altered in number and morphology in a variety of neurological and psychiatric diseases linked to maldevelopment. In the present study we show that reelin-positive CR cells persist in the layer I of the entorhinal cortex in normal senescent brains and are also preserved in AD. The majority of CR cells in AD is morphologically and cytochemically-as revealed by double labeling with calcium-binding proteins-indistinguishable from normal cases, suggesting that they are not dramatically altered in the entorhinal cortex of AD patients. Nevertheless, CR cells seem to be partially affected by the formation of paired helical filaments, indicating subtle changes that are suggested to be a result rather than a cause of the pathogenetic cascade of AD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0001-6322
pubmed:author
pubmed:issnType
Print
pubmed:volume
106
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
291-302
pubmed:dateRevised
2011-8-2
pubmed:meshHeading
pubmed-meshheading:12811583-Aged, pubmed-meshheading:12811583-Aged, 80 and over, pubmed-meshheading:12811583-Aging, pubmed-meshheading:12811583-Alzheimer Disease, pubmed-meshheading:12811583-Amyloid beta-Peptides, pubmed-meshheading:12811583-Animals, pubmed-meshheading:12811583-Antibodies, Monoclonal, pubmed-meshheading:12811583-Calcium-Binding Proteins, pubmed-meshheading:12811583-Cell Adhesion Molecules, Neuronal, pubmed-meshheading:12811583-Cell Count, pubmed-meshheading:12811583-Cerebral Ventricles, pubmed-meshheading:12811583-Entorhinal Cortex, pubmed-meshheading:12811583-Extracellular Matrix Proteins, pubmed-meshheading:12811583-Female, pubmed-meshheading:12811583-Humans, pubmed-meshheading:12811583-Immunohistochemistry, pubmed-meshheading:12811583-Male, pubmed-meshheading:12811583-Mice, pubmed-meshheading:12811583-Nerve Tissue Proteins, pubmed-meshheading:12811583-Neurons, pubmed-meshheading:12811583-Serine Endopeptidases
pubmed:year
2003
pubmed:articleTitle
Reelin-immunoreactive Cajal-Retzius cells: the entorhinal cortex in normal aging and Alzheimer's disease.
pubmed:affiliation
Department of Neuroanatomy, Paul Flechsig Institute for Brain Research, University of Leipzig, Jahnallee 59, 04109 Leipzig, Germany. rieda@medizin.uni-leipzig.de
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't