Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-2-12
pubmed:abstractText
Progressive supranuclear palsy (PSP) typically presents with a gradual onset and progressive course of symmetric levodopa-unresponsive parkinsonism characterized by postural instability with falls, supranuclear vertical gaze palsy, dysarthria, dysphagia, and cognitive and behavioral disturbances. Though the clinical course is variable, the typical presentation is usually associated with mortality at 5-9 years after symptom onset. The pathological hallmark of PSP is widespread neuronal cell loss with deposition of aggregated hyperphosphorylated tau, particularly within the midbrain. Etiology remains elusive, but a variable combination of genetic, environmental, oxidative stress, and inflammatory factors may all contribute. Genetic advances have confirmed the H1 tau haplotype on chromosome 17q21.31 to be associated with PSP, while the H2 haplotype seems protective. With greater knowledge of the molecular and genetic aspects of PSP, we can expect future diagnostic and therapeutic challenges to be more effectively met.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1353-8020
pubmed:author
pubmed:issnType
Print
pubmed:volume
13 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S341-6
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Unraveling progressive supranuclear palsy: from the bedside back to the bench.
pubmed:affiliation
Division of Movement Disorders, Department of Neurology, University of Louisville, Louisville, KY, USA. david.houghton@louisville.edu
pubmed:publicationType
Journal Article, Review