Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2004-10-12
pubmed:abstractText
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1526-632X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
12
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1155-62
pubmed:dateRevised
2005-12-27
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
A focus on the synapse for neuroprotection in Alzheimer disease and other dementias.
pubmed:affiliation
Center for Aging and Developmental Biology, University of Rochester School of Medicine, Rochester, NY 14642-8673, USA.
pubmed:publicationType
Journal Article, Review