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Depositordc.contributorSpires-Jones, Tara
Funderdc.contributor.otherAlzheimer's Research UKen_UK
Funderdc.contributor.otherScottish Governmenten_UK
Funderdc.contributor.otherWellcome Trusten_UK
Data Creatordc.creatorSpires-Jones, Tara L
Data Creatordc.creatorJackson, Rosemary J
Date Accessioneddc.date.accessioned2016-10-27T09:08:16Z
Date Availabledc.date.available2016-10-28T04:15:30Z
Citationdc.identifier.citationSpires-Jones, Tara; Jackson, Rosemary. (2016). Human tau increases amyloid beta plaque size but not amyloid beta-mediated synapse loss in a novel mouse model of Alzheimer’s disease: Data set from Jackson et al 2016 EJN, [dataset]. https://doi.org/10.7488/ds/1507.en
Persistent Identifierdc.identifier.urihttp://hdl.handle.net/10283/2133
Persistent Identifierdc.identifier.urihttps://doi.org/10.7488/ds/1507
Dataset Description (abstract)dc.description.abstractAlzheimer’s disease is characterized by the presence of aggregates of amyloid beta (Aβ) in senile plaques and tau in neurofibrillary tangles, as well as marked neuron and synapse loss. Of these pathological changes, synapse loss correlates most strongly with cognitive decline. Synapse loss occurs prominently around plaques due to accumulations of oligomeric Aβ. Recent evidence suggests that tau may also play a role in synapse loss but the interactions of Aβ and tau in synapse loss remain to be determined. In this study, we generated a novel transgenic mouse line, the APP/PS1/rTg21221 line, by crossing APP/PS1 mice, which develop Aβ-plaques and synapse loss, with rTg21221 mice, which overexpress wild-type human tau. When compared to the APP/PS1 mice without human tau, the cross-sectional area of ThioS+ dense core plaques was increased by ~50%. Along with increased plaque size, we observed an increase in plaque-associated dystrophic neurites containing misfolded tau, but there was no exacerbation of neurite curvature or local neuron loss around plaques. Array tomography analysis similarly revealed no worsening of synapse loss around plaques, and no change in the accumulation of Aβ at synapses. Together, these results indicate that adding human wild-type tau exacerbates plaque pathology and neurite deformation but does not exacerbate plaque-associated synapse loss. This dataset includes data associated with this manuscript along with custom analysis macros. The raw images are too large to upload to our limited repository system, at over 300 GB total, but are available upon request tara.spires-jones@ed.ac.uken_UK
Languagedc.language.isoengen_UK
Relation (Is Referenced By)dc.relation.isreferencedbyhttps://doi.org/10.1111/ejn.13442en_UK
Relation (Is Referenced By)dc.relation.isreferencedbyJackson, R. J., Rudinskiy, N., Herrmann, A. G., Croft, S., Kim, J. M., Petrova, V., Ramos-Rodriguez, J. J., Pitstick, R., Wegmann, S., Garcia-Alloza, M., Carlson, G. A., Hyman, B. T. and Spires-Jones, T. L. (2016), Human tau increases amyloid β plaque size but not amyloid β-mediated synapse loss in a novel mouse model of Alzheimer's disease. Eur J Neurosci, 44: 3056–3066. doi:10.1111/ejn.13442en
Rightsdc.rightsCreative Commons Attribution 4.0 International Public Licenseen
Subjectdc.subjectAlzheimeren_UK
Subjectdc.subjectsynapseen_UK
Subject Classificationdc.subject.classificationSubjects allied to Medicine::Neuroscienceen_UK
Titledc.titleHuman tau increases amyloid beta plaque size but not amyloid beta-mediated synapse loss in a novel mouse model of Alzheimer’s disease: Data set from Jackson et al 2016 EJNen_UK
Typedc.typedataseten_UK

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