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http://hdl.handle.net/1942/30284
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DC Field | Value | Language |
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dc.contributor.author | TERWEL, Dick | - |
dc.contributor.author | Muyllaert, David | - |
dc.contributor.author | DEWACHTER, Ilse | - |
dc.contributor.author | Borghgraef, Peter | - |
dc.contributor.author | Devijver, Herman | - |
dc.contributor.author | Croes, Sophie | - |
dc.contributor.author | Van Leuven, Fred | - |
dc.date.accessioned | 2020-01-10T11:55:39Z | - |
dc.date.available | 2020-01-10T11:55:39Z | - |
dc.date.issued | 2008 | - |
dc.date.submitted | 2020-01-09T11:50:04Z | - |
dc.identifier.citation | The American journal of pathology, 172 (3) , p. 786 -798 | - |
dc.identifier.uri | http://hdl.handle.net/1942/30284 | - |
dc.description.abstract | The hypothesis that amyloid pathology precedes and induces the tau pathology of Alzheimer's disease is experimentally supported here through the identification of GSK-3 isozymes as a major link in the signaling pathway from amyloid to tau pathology. This study compares two novel bigenic mouse models: APP-V717I x Tau-P301L mice with combined amyloid and tau pathology and GSK-3beta x Tau-P301L mice with tauopathy only. Extensive and remarkable parallels were observed between these strains including 1) aggravation of tauopathy with highly fibrillar tangles in the hippocampus and cortex; 2) prolonged survival correlated to alleviated brainstem tauopathy; 3) development of severe cognitive and behavioral defects in young adults before the onset of amyloid deposition or tauopathy; and 4) presence of pathological phospho-epitopes of tau, including the characteristic GSK-3beta motif at S396/S404. Both GSK-3 isozymes were activated in the brain of parental APP-V717I amyloid mice, even at a young age when cognitive and behavioral defects are evident but before amyloid deposition. The data indicate that amyloid induces tauopathy through activation of GSK-3 and suggest a role for the kinase in maintaining the functional integrity of adult neurons. | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC INVESTIGATIVE PATHOLOGY, INC | - |
dc.rights | American Society for Investigative Pathology | - |
dc.subject.other | Glycogen-Synthase Kinase-3-Beta | - |
dc.subject.other | Long-Term Potentiation | - |
dc.subject.other | Transgenic Mice | - |
dc.subject.other | Alzheimers-Disease | - |
dc.subject.other | Tau-Protein | - |
dc.subject.other | Neurofibrillary Tangles | - |
dc.subject.other | Precursor Protein | - |
dc.subject.other | Beta Peptides | - |
dc.subject.other | A-Beta | - |
dc.subject.other | Phosphorylation | - |
dc.title | Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice | - |
dc.type | Journal Contribution | - |
dc.identifier.epage | 798 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 786 | - |
dc.identifier.volume | 172 | - |
local.bibliographicCitation.jcat | A1 | - |
local.publisher.place | 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA | - |
local.type.refereed | Refereed | - |
local.type.specified | Article | - |
dc.source.type | Article | - |
dc.identifier.doi | 10.2353/ajpath.2008.070904 | - |
dc.identifier.pmid | 18258852 | - |
dc.identifier.isi | 000253616400022 | - |
local.provider.type | PubMed | - |
local.uhasselt.uhpub | no | - |
item.fullcitation | TERWEL, Dick; Muyllaert, David; DEWACHTER, Ilse; Borghgraef, Peter; Devijver, Herman; Croes, Sophie & Van Leuven, Fred (2008) Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice. In: The American journal of pathology, 172 (3) , p. 786 -798. | - |
item.accessRights | Restricted Access | - |
item.fulltext | With Fulltext | - |
item.contributor | TERWEL, Dick | - |
item.contributor | Muyllaert, David | - |
item.contributor | DEWACHTER, Ilse | - |
item.contributor | Borghgraef, Peter | - |
item.contributor | Devijver, Herman | - |
item.contributor | Croes, Sophie | - |
item.contributor | Van Leuven, Fred | - |
Appears in Collections: | Research publications |
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1-s2.0-S0002944010618408-main.pdf Restricted Access | Published version | 2 MB | Adobe PDF | View/Open Request a copy |
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