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dc.contributor.authorMallucci, Giovannaen
dc.contributor.authorKlenerman, Daviden
dc.contributor.authorRubinsztein, Daviden
dc.date.accessioned2020-10-12T23:31:14Z
dc.date.available2020-10-12T23:31:14Z
dc.date.issued2020-10en
dc.identifier.issn1081-0706
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/311394
dc.description.abstractAs the world's population ages, neurodegenerative disorders are poised to become the commonest cause of death. Despite this, they remain essentially untreatable. Characterized pathologically both by the aggregation of disease-specific misfolded proteins and by changes in cellular stress responses, to date, therapeutic approaches have focused almost exclusively on reducing misfolded protein load-notably amyloid beta (Aβ) in Alzheimer's disease. The repeated failure of clinical trials has led to despondency over the possibility that these disorders will ever be treated. We argue that this is in fact a time for optimism: Targeting various generic stress responses is emerging as an increasingly promising means of modifying disease progression across these disorders. New treatments are approaching clinical trials, while novel means of targeting aggregates could eventually act preventively in early disease.
dc.description.sponsorshipWe are grateful for funding from the UK Dementia Research Institute (funded by the MedicalResearch Council UK, Alzheimer’s Research UK, and the Alzheimer’s Society) (G.R.M., D.K.,and D.C.R.); the Cambridge Centre for Parkinson-Plus (G.R.M. and D.C.R.); the European Re-search Council, the Medical Research Council, the Joint Programme Neurodegenerative Disease,the Centres of Excellence in Neurodegeneration, and the Wellcome Trust Collaborative Award(G.R.M.); the Roger de Spoelberch Foundation, Alzheimer’s Research UK, and the National In-stitute for Health Research Cambridge Biomedical Research Centre (D.C.R.); and The RoyalSociety (D.K.).
dc.format.mediumPrinten
dc.languageengen
dc.rightsAll rights reserved
dc.rights.uri
dc.subjectLysosomesen
dc.subjectAnimalsen
dc.subjectHumansen
dc.subjectNeurodegenerative Diseasesen
dc.subjectStress, Physiologicalen
dc.subjectUnfolded Protein Responseen
dc.subjectProtein Aggregatesen
dc.subjectAutophagosomesen
dc.titleDeveloping Therapies for Neurodegenerative Disorders: Insights from Protein Aggregation and Cellular Stress Responses.en
dc.typeArticle
prism.endingPage189
prism.publicationDate2020en
prism.publicationNameAnnual review of cell and developmental biologyen
prism.startingPage165
prism.volume36en
dc.identifier.doi10.17863/CAM.58484
dcterms.dateAccepted2020-06-08en
rioxxterms.versionofrecord10.1146/annurev-cellbio-040320-120625en
rioxxterms.versionAM
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2020-10en
dc.contributor.orcidMallucci, Giovanna [0000-0001-8504-1191]
dc.contributor.orcidKlenerman, David [0000-0001-7116-6954]
dc.contributor.orcidRubinsztein, David [0000-0001-5002-5263]
dc.identifier.eissn1530-8995
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idRoyal Society (RP150066)
pubs.funder-project-idECH2020 EUROPEAN RESEARCH COUNCIL (ERC) (647479)
pubs.funder-project-idWellcome Trust (via MRC) (201487/Z/16/Z)
pubs.funder-project-idUK Dementia Research Institute (DRICam17/18)
pubs.funder-project-idMRC (MR/R024820/1)
pubs.funder-project-idMRC (MR/S00503X/1)
rioxxterms.freetoread.startdate2100-01-01


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