Linked Life Data

17071137

Source:http://linkedlifedata.com/resource/pubmed/id/17071137

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-1-23
pubmed:abstractText
Huntington's disease (HD) is a late-onset neurodegenerative disorder that follows an autosomal-dominant pattern of inheritance. In human cases of HD and experimental models of the disease, multiple alterations in neurotransmitters and post-receptor machineries have been described. Dopamine, acetylcholine and glutamate signalling, which usually cooperate in the induction of physiological synaptic plasticity, are all disrupted. Impairment of the induction and reversal of the main forms of neuronal synaptic plasticity influences the computational function of complex neural circuits that mediate essential cognitive and motor functions. As long-term potentiation and long-term depression represent the accepted model for neuronal learning processes, their impairment could account for the onset and progression of both motor and cognitive symptoms of HD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1471-4892
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
106-11
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Plastic abnormalities in experimental Huntington's disease.
pubmed:affiliation
Clinica Neurologica, Università degli Studi di Perugia, Ospedale S. Maria della Misericordia, Via S Andrea delle Fratte, 06156, Perugia, Italy; IRCCS Fondazione Santa Lucia, Rome, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't