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dc.contributor.authorBevan Jones, WR
dc.contributor.authorCope, TE
dc.contributor.authorPassamonti, L
dc.contributor.authorFryer, TD
dc.contributor.authorHong, YT
dc.contributor.authorAigbirhio, F
dc.contributor.authorKril, JJ
dc.contributor.authorForrest, SL
dc.contributor.authorAllinson, K
dc.contributor.authorColes, JP
dc.contributor.authorSpillantini, MG
dc.contributor.authorHodges, JR
dc.contributor.authorO'Brien, JT
dc.contributor.authorRowe, JB
dc.date.accessioned2018-12-12
dc.date.available2018-12-12
dc.date.issued2016-10-18
dc.identifier.citationBevan Jones WR, Cope TE, Passamonti L, et al. [18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation. Ann Clin Transl Neurol. 2016;3(12):940-947. Published 2016 Oct 18. doi:10.1002/acn3.366en_AU
dc.identifier.urihttp://hdl.handle.net/2123/19650
dc.description.abstractThe validation of tau radioligands could improve the diagnosis of frontotemporal lobar degeneration and the assessment of disease-modifying therapies. Here, we demonstrate that binding of the tau radioligand [18F]AV-1451 was significantly abnormal in both magnitude and distribution in a patient with familial frontotemporal dementia due to a MAPT 10 + 16C>T gene mutation, recapitulating the pattern of neuropathology seen in her father. Given the genetic diagnosis and the non-Alzheimer's pathology, these findings suggest that [18F]AV-1451 might be a useful biomarker in primary tauopathies. Largerscale in vivo and post-mortem studies will be needed to assess the technique's specificity.en_AU
dc.description.sponsorshipNHMRC RGMS ID P02919571en_AU
dc.language.isoen_AUen_AU
dc.publisherAnn Clin Transl Neurolen_AU
dc.relationNHMRC RGMS ID P02919571en_AU
dc.rightsCC BY 4.0en_AU
dc.subjectNeuropathologyen_AU
dc.title[18F]AV-1451 PET in behavioural variant frontotemporal dementia due to MAPT mutationen_AU
dc.typeArticleen_AU
dc.identifier.doihttp://dx.doi.org/10.1002/acn3.366
dc.type.pubtypePublisher's versionen_AU


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