Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-9-8
pubmed:abstractText
Neurofibrillary tangles (NFTs) are a pathological hallmark of many neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP17). However, the cellular origin and the consequence of the NFT formation are poorly understood. Epidemiological evidence suggests a much higher occurrence of dementia in stroke patients. This may represent the pathogenesis of sporadic AD, which accounts for the majority of AD occurrence. Here we show that after a transient cerebral ischemia, hyperphosphorylated tau accumulates in cortical neurons in a site-specific manner. The hyperphosphorylated tau presents a conformation similar to those present in human tauopathies, and colocalizes largely with signs of apoptosis. Our current study suggests that tau hyperphosphorylation may contribute to the brain damage induced by transient cerebral ischemia, and may be involved in the pathogenesis of neurodegenerative disorders in patients after stroke. Further, these results indicate that ischemic neuronal damage and apoptosis associates with tau hyperphosphorylation, and potentially NFTs formation. Finally, our results also suggest that neuronal apoptosis may be a therapeutic target in preventing tauopathy-related neurodegenerative diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
1022
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
30-8
pubmed:dateRevised
2011-8-2
pubmed:meshHeading
pubmed-meshheading:15353210-Analysis of Variance, pubmed-meshheading:15353210-Animals, pubmed-meshheading:15353210-Antibodies, Monoclonal, pubmed-meshheading:15353210-Blotting, Western, pubmed-meshheading:15353210-Cell Death, pubmed-meshheading:15353210-Disease Models, Animal, pubmed-meshheading:15353210-Female, pubmed-meshheading:15353210-Frontal Lobe, pubmed-meshheading:15353210-Functional Laterality, pubmed-meshheading:15353210-Immunohistochemistry, pubmed-meshheading:15353210-In Situ Nick-End Labeling, pubmed-meshheading:15353210-Indoles, pubmed-meshheading:15353210-Ischemic Attack, Transient, pubmed-meshheading:15353210-Nerve Tissue Proteins, pubmed-meshheading:15353210-Neurons, pubmed-meshheading:15353210-Phosphorylation, pubmed-meshheading:15353210-Rats, pubmed-meshheading:15353210-Tetrazolium Salts, pubmed-meshheading:15353210-tau Proteins
pubmed:year
2004
pubmed:articleTitle
Transient cerebral ischemia induces site-specific hyperphosphorylation of tau protein.
pubmed:affiliation
Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro