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dc.contributor.authorRobbins, Miranda
dc.contributor.authorClayton, Emma
dc.contributor.authorKaminski, Gabriele
dc.date.accessioned2021-11-06T00:31:38Z
dc.date.available2021-11-06T00:31:38Z
dc.date.issued2021-09-09
dc.identifier.issn2051-5960
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/330380
dc.description.abstractIn this review, we discuss the synaptic aspects of Tau pathology occurring during Alzheimer's disease (AD) and how this may relate to memory impairment, a major hallmark of AD. Whilst the clinical diagnosis of AD patients is a loss of working memory and long-term declarative memory, the histological diagnosis is the presence of neurofibrillary tangles of hyperphosphorylated Tau and Amyloid-beta plaques. Tau pathology spreads through synaptically connected neurons to impair synaptic function preceding the formation of neurofibrillary tangles, synaptic loss, axonal retraction and cell death. Alongside synaptic pathology, recent data suggest that Tau has physiological roles in the pre- or post- synaptic compartments. Thus, we have seen a shift in the research focus from Tau as a microtubule-stabilising protein in axons, to Tau as a synaptic protein with roles in accelerating spine formation, dendritic elongation, and in synaptic plasticity coordinating memory pathways. We collate here the myriad of emerging interactions and physiological roles of synaptic Tau, and discuss the current evidence that synaptic Tau contributes to pathology in AD.
dc.description.sponsorshipG.S.K.S. acknowledges funding from the Wellcome Trust (065807/Z/01/Z) (203249/Z/16/Z), the UK Medical Research Council (MRC) (MR/K02292X/1), Alzheimer Research UK (ARUK) (ARUK-PG013-14), Michael J Fox Foundation (16238) and Infnitus China Ltd. M.A.R acknowledges funding from the Engineering and Physical Sciences Research Council (EP/L015889/1).
dc.languageeng
dc.publisherBioMed Central
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAlzheimer’s disease
dc.subjectMemory
dc.subjectNeurodegeneration
dc.subjectPlasticity
dc.subjectSynapses
dc.subjectTau
dc.titleSynaptic tau: A pathological or physiological phenomenon?
dc.typeArticle
prism.endingPage149
prism.issueIdentifier1
prism.publicationNameActa Neuropathologica Communications
prism.startingPage149
prism.volume9
dc.identifier.doi10.17863/CAM.77823
dcterms.dateAccepted2021-08-12
rioxxterms.versionofrecord10.1186/s40478-021-01246-y
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2021-08-12
dc.contributor.orcidKaminski, Gabriele [0000-0002-1843-2202]
dc.identifier.eissn2051-5960
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MR/K02292X/1)
pubs.funder-project-idWellcome Trust (065807/Z/01/Z)
pubs.funder-project-idEngineering and Physical Sciences Research Council (EP/L015889/1)
pubs.funder-project-idWellcome Trust (203249/Z/16/Z)
cam.issuedOnline2021-11-09


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International