Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/39903
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dc.contributor.authorSchreiber, Stefanie-
dc.contributor.authorWilisch-Neumann, Annette-
dc.contributor.authorSchreiber, Frank-
dc.contributor.authorAssmann, Anne-
dc.contributor.authorScheumann, Vincent-
dc.contributor.authorPerosa, Valentina-
dc.contributor.authorJandke, Solveig-
dc.contributor.authorMawrin, Christian-
dc.contributor.authorCarare, Roxana O.-
dc.contributor.authorWerring, David J.-
dc.date.accessioned2021-12-02T13:36:02Z-
dc.date.available2021-12-02T13:36:02Z-
dc.date.issued2020-
dc.date.submitted2020-
dc.identifier.urihttps://opendata.uni-halle.de//handle/1981185920/41858-
dc.identifier.urihttp://dx.doi.org/10.25673/39903-
dc.description.abstractDeep perforator arteriopathy (DPA) and cerebral amyloid angiopathy (CAA) are the commonest known cerebral small vessel diseases (CSVD), which cause ischaemic stroke, intracebral haemorrhage (ICH) and vascular cognitive impairment (VCI). While thus far mainly considered as separate entities, we here propose that DPA and CAA share similarities, overlap and interact, so that ‘pure’ DPA or CAA are extremes along a continuum of age-related small vessel pathologies. We suggest blood-brain barrier (BBB) breakdown, endothelial damage and impaired perivascular β-amyloid (Aβ) drainage are hallmark common mechanisms connecting DPA and CAA. We also suggest a need for new biomarkers (e.g. high-resolution imaging) to deepen understanding of the complex relationships between DPA and CAA.eng
dc.description.sponsorshipProjekt DEAL 2019-
dc.language.isoeng-
dc.relation.ispartofhttps://doi.org/10.1111/(ISSN)1365-2990-
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/-
dc.subjectDeep perforator arteriopathy (DPA)eng
dc.subjectAmyloid vasculopathieseng
dc.subjectNonamyloid vasculopathieseng
dc.subject.ddc610.72-
dc.titleInvited review : the spectrum of age‐related small vessel diseases : potential overlap and interactions of amyloid and nonamyloid vasculopathieseng
dc.typeArticle-
dc.identifier.urnurn:nbn:de:gbv:ma9:1-1981185920-418588-
local.versionTypepublishedVersion-
local.bibliographicCitation.journaltitleNeuropathology & applied neurobiology-
local.bibliographicCitation.volume46-
local.bibliographicCitation.issue3-
local.bibliographicCitation.pagestart219-
local.bibliographicCitation.pageend239-
local.bibliographicCitation.publishernameWiley-Blackwell-
local.bibliographicCitation.publisherplaceOxford [u.a.]-
local.bibliographicCitation.doi10.1111/nan.12576-
local.openaccesstrue-
dc.identifier.ppn1681498014-
local.bibliographicCitation.year2020-
cbs.sru.importDate2021-12-02T13:30:57Z-
local.bibliographicCitationEnthalten in Neuropathology & applied neurobiology - Oxford [u.a.] : Wiley-Blackwell, 1975-
local.accessrights.dnbfree-
Appears in Collections:Medizinische Fakultät (OA)

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