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dc.contributor.author Papp Mátyás, Imre
dc.contributor.author Kovács, Tibor
dc.date.accessioned 2015-02-04T10:55:07Z
dc.date.available 2015-02-04T10:55:07Z
dc.date.issued 2013
dc.identifier 84888042679
dc.identifier.citation pagination=818-828; journalVolume=10; journalIssueNumber=8; journalTitle=CURRENT ALZHEIMER RESEARCH;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/1271
dc.identifier.uri doi:10.2174/15672050113109990153
dc.description.abstract In Alzheimer's disease (AD), neurofibrillary degeneration in the hemispheres starts in the limbic and paralimbic regions prior to those in the isocortical ones but factors determining the progression of these changes are unknown. Previous studies have shown that migration of extracellular substances (volume transmission) driven by arterial pulse pressure waves from the cerebrospinal fluid (CSF) towards the brain parenchyma occurs earlier in these limbic and paralimbic cortices located around the basal cisterns containing the proximal segments of the main hemispheric arteries than in the isocortex. Considering this similarity, the aim of our study was to examine the relation between the proximal segments of the main hemispheric arteries and the development and spread of neurofibrillary tangles (NFTs) in limbic and early isocortical Braaks' stages. Blocks following proximosdistal levels of the anterior and middle cerebral arteries containing areas of the cingulate and insular cortices, respectively, were dissected and NFTs were counted. In both regions, the density of NFTs decreased in parallel with the proximodistal segments of the accompanying arteries. Our results show that neurofibrillary degeneration in AD is related to the proximodistal levels of the main hemispheric arteries and raise the possibility that this effect is mediated by volume transmission from the CSF into the brain.
dc.relation.ispartof urn:issn:1567-2050
dc.title Progression of Alzheimer-type Neurofibrillary Tangles is Related to the Proximodistal Segments of the Hemispheric Arteries.
dc.type Journal Article
dc.date.updated 2015-01-29T08:57:26Z
dc.language.rfc3066 en
dc.identifier.mtmt 2444282
dc.identifier.wos 000324864400005
dc.identifier.pubmed 23919772
dc.contributor.department SE/AOK/K/Neurológiai Klinika
dc.contributor.institution Semmelweis Egyetem


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