{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,12]],"date-time":"2026-11-12T12:17:26Z","timestamp":1794485846901,"version":"4.9.1"},"reference-count":148,"publisher":"Springer Science and Business Media LLC","issue":"6","license":[{"start":{"date-parts":[[2021,6,1]],"date-time":"2021-06-01T00:00:00Z","timestamp":1622505600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.springer.com\/tdm"},{"start":{"date-parts":[[2021,6,1]],"date-time":"2021-06-01T00:00:00Z","timestamp":1622505600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.springer.com\/tdm"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Nat Med"],"published-print":{"date-parts":[[2021,6]]},"DOI":"10.1038\/s41591-021-01382-x","type":"journal-article","created":{"date-parts":[[2021,6,3]],"date-time":"2021-06-03T12:03:27Z","timestamp":1622721807000},"page":"954-963","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1145,"title":["Biomarkers for neurodegenerative diseases"],"prefix":"10.1038","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8467-7286","authenticated-orcid":false,"given":"Oskar","family":"Hansson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,6,3]]},"reference":[{"key":"1382_CR1","doi-asserted-by":"crossref","unstructured":"GBD 2016 Dementia Collaborators. Global, regional, and national burden of Alzheimer\u2019s disease and other dementias, 1990\u20132016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 18, 88\u2013106 (2019).","DOI":"10.1016\/S1474-4422(18)30403-4"},{"key":"1382_CR2","unstructured":"Prince, M. et al. World Alzheimer Report 2015. The Global Impact of Dementia: An Analysis of Prevalence, Incidence, Cost and Trends. https:\/\/www.alzint.org\/u\/WorldAlzheimerReport2015.pdf (Alzheimer\u2019s Disease International, 2015)."},{"key":"1382_CR3","doi-asserted-by":"crossref","first-page":"1106","DOI":"10.1016\/S1474-4422(07)70291-0","volume":"6","author":"S Seshadri","year":"2007","unstructured":"Seshadri, S. & Wolf, P. A. Lifetime risk of stroke and dementia: current concepts, and estimates from the Framingham Study. Lancet Neurol. 6, 1106\u20131114 (2007).","journal-title":"Lancet Neurol."},{"key":"1382_CR4","doi-asserted-by":"crossref","first-page":"98","DOI":"10.1001\/archgenpsychiatry.2011.155","volume":"69","author":"P Buchhave","year":"2012","unstructured":"Buchhave, P. et al. Cerebrospinal fluid levels of \u03b2-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia. Arch. Gen. Psychiatry 69, 98\u2013106 (2012).","journal-title":"Arch. Gen. Psychiatry"},{"key":"1382_CR5","doi-asserted-by":"crossref","first-page":"241","DOI":"10.1016\/S1474-4422(18)30028-0","volume":"17","author":"BA Gordon","year":"2018","unstructured":"Gordon, B. A. et al. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer\u2019s disease: a longitudinal study. Lancet Neurol. 17, 241\u2013250 (2018).","journal-title":"Lancet Neurol."},{"key":"1382_CR6","doi-asserted-by":"crossref","first-page":"357","DOI":"10.1016\/S1474-4422(13)70044-9","volume":"12","author":"VL Villemagne","year":"2013","unstructured":"Villemagne, V. L. et al. Amyloid \u03b2 deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer\u2019s disease: a prospective cohort study. Lancet Neurol. 12, 357\u2013367 (2013).","journal-title":"Lancet Neurol."},{"key":"1382_CR7","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1186\/s13024-019-0333-5","volume":"14","author":"MA DeTure","year":"2019","unstructured":"DeTure, M. A. & Dickson, D. W. The neuropathological diagnosis of Alzheimer\u2019s disease. Mol. Neurodegener. 14, 32 (2019).","journal-title":"Mol. Neurodegener."},{"key":"1382_CR8","doi-asserted-by":"crossref","first-page":"199","DOI":"10.1038\/s41582-020-0333-7","volume":"16","author":"C Peng","year":"2020","unstructured":"Peng, C., Trojanowski, J. Q. & Lee, V. M. Protein transmission in neurodegenerative disease. Nat. Rev. Neurol. 16, 199\u2013212 (2020).","journal-title":"Nat. Rev. Neurol."},{"key":"1382_CR9","doi-asserted-by":"crossref","unstructured":"Braak, H. & Del Tredici, K. Potential pathways of abnormal tau and \u03b1-synuclein dissemination in sporadic Alzheimer\u2019s and Parkinson\u2019s diseases. Cold Spring Harb. Perspect. Biol. 8, a023630 (2016).","DOI":"10.1101\/cshperspect.a023630"},{"key":"1382_CR10","doi-asserted-by":"crossref","first-page":"353","DOI":"10.1126\/science.1072994","volume":"297","author":"J Hardy","year":"2002","unstructured":"Hardy, J. & Selkoe, D. J. The amyloid hypothesis of Alzheimer\u2019s disease: progress and problems on the road to therapeutics. Science 297, 353\u2013356 (2002).","journal-title":"Science"},{"key":"1382_CR11","doi-asserted-by":"crossref","first-page":"603","DOI":"10.1016\/j.cell.2015.12.056","volume":"164","author":"B De Strooper","year":"2016","unstructured":"De Strooper, B. & Karran, E. The cellular phase of Alzheimer\u2019s disease. Cell 164, 603\u2013615 (2016).","journal-title":"Cell"},{"key":"1382_CR12","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1186\/alzrt59","volume":"3","author":"RJ Bateman","year":"2011","unstructured":"Bateman, R. J. et al. Autosomal-dominant Alzheimer\u2019s disease: a review and proposal for the prevention of Alzheimer\u2019s disease. Alzheimers Res. Ther. 3, 1 (2011).","journal-title":"Alzheimers Res. Ther."},{"key":"1382_CR13","doi-asserted-by":"crossref","first-page":"1672","DOI":"10.1016\/S0140-6736(15)00461-4","volume":"386","author":"J Bang","year":"2015","unstructured":"Bang, J., Spina, S. & Miller, B. L. Frontotemporal dementia. Lancet 386, 1672\u20131682 (2015).","journal-title":"Lancet"},{"key":"1382_CR14","doi-asserted-by":"crossref","first-page":"896","DOI":"10.1016\/S0140-6736(14)61393-3","volume":"386","author":"LV Kalia","year":"2015","unstructured":"Kalia, L. V. & Lang, A. E. Parkinson\u2019s disease. Lancet 386, 896\u2013912 (2015).","journal-title":"Lancet"},{"key":"1382_CR15","doi-asserted-by":"crossref","first-page":"137","DOI":"10.1007\/s00441-017-2706-9","volume":"373","author":"MG Spillantini","year":"2018","unstructured":"Spillantini, M. G. & Goedert, M. Neurodegeneration and the ordered assembly of \u03b1-synuclein. Cell Tissue Res. 373, 137\u2013148 (2018).","journal-title":"Cell Tissue Res."},{"key":"1382_CR16","doi-asserted-by":"crossref","first-page":"88","DOI":"10.1212\/WNL.0000000000004058","volume":"89","author":"IG McKeith","year":"2017","unstructured":"McKeith, I. G. et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium. Neurology 89, 88\u2013100 (2017).","journal-title":"Neurology"},{"key":"1382_CR17","doi-asserted-by":"crossref","first-page":"1683","DOI":"10.1016\/S0140-6736(15)00462-6","volume":"386","author":"Z Walker","year":"2015","unstructured":"Walker, Z., Possin, K. L., Boeve, B. F. & Aarsland, D. Lewy body dementias. Lancet 386, 1683\u20131697 (2015).","journal-title":"Lancet"},{"key":"1382_CR18","doi-asserted-by":"crossref","first-page":"887","DOI":"10.1016\/j.jalz.2015.06.1889","volume":"11","author":"CA Hunter","year":"2015","unstructured":"Hunter, C. A. et al. Medical costs of Alzheimer\u2019s disease misdiagnosis among US Medicare beneficiaries. Alzheimers Dement. 11, 887\u2013895 (2015).","journal-title":"Alzheimers Dement."},{"key":"1382_CR19","doi-asserted-by":"crossref","first-page":"1143","DOI":"10.1212\/WNL.56.9.1143","volume":"56","author":"DS Knopman","year":"2001","unstructured":"Knopman, D. S. et al. Practice parameter: diagnosis of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 56, 1143\u20131153 (2001).","journal-title":"Neurology"},{"key":"1382_CR20","doi-asserted-by":"crossref","first-page":"358","DOI":"10.1136\/jnnp-2017-316844","volume":"89","author":"G Rizzo","year":"2018","unstructured":"Rizzo, G. et al. Accuracy of clinical diagnosis of dementia with Lewy bodies: a systematic review and meta-analysis. J. Neurol. Neurosurg. Psychiatry 89, 358\u2013366 (2018).","journal-title":"J. Neurol. Neurosurg. Psychiatry"},{"key":"1382_CR21","doi-asserted-by":"crossref","first-page":"266","DOI":"10.1097\/NEN.0b013e31824b211b","volume":"71","author":"TG Beach","year":"2012","unstructured":"Beach, T. G., Monsell, S. E., Phillips, L. E. & Kukull, W. Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005\u20132010. J. Neuropathol. Exp. Neurol. 71, 266\u2013273 (2012).","journal-title":"J. Neuropathol. Exp. Neurol."},{"key":"1382_CR22","doi-asserted-by":"crossref","first-page":"306","DOI":"10.1097\/WAD.0b013e3181a6bebc","volume":"23","author":"A Bradford","year":"2009","unstructured":"Bradford, A., Kunik, M. E., Schulz, P., Williams, S. P. & Singh, H. Missed and delayed diagnosis of dementia in primary care: prevalence and contributing factors. Alzheimer Dis. Assoc. Disord. 23, 306\u2013314 (2009).","journal-title":"Alzheimer Dis. Assoc. Disord."},{"key":"1382_CR23","doi-asserted-by":"crossref","first-page":"2227","DOI":"10.1056\/NEJMcp0910237","volume":"364","author":"RC Petersen","year":"2011","unstructured":"Petersen, R. C. Clinical practice. Mild cognitive impairment. N. Engl. J. Med. 364, 2227\u20132234 (2011).","journal-title":"N. Engl. J. Med."},{"key":"1382_CR24","doi-asserted-by":"crossref","first-page":"566","DOI":"10.1212\/WNL.0000000000002350","volume":"86","author":"G Rizzo","year":"2016","unstructured":"Rizzo, G. et al. Accuracy of clinical diagnosis of Parkinson disease: a systematic review and meta-analysis. Neurology 86, 566\u2013576 (2016).","journal-title":"Neurology"},{"key":"1382_CR25","doi-asserted-by":"crossref","first-page":"171","DOI":"10.1002\/mds.27872","volume":"35","author":"G Respondek","year":"2020","unstructured":"Respondek, G. et al. Validation of the Movement Disorder Society criteria for the diagnosis of 4-repeat tauopathies. Mov. Disord. 35, 171\u2013176 (2020).","journal-title":"Mov. Disord."},{"key":"1382_CR26","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1097\/WAD.0000000000000144","volume":"30","author":"J Sevigny","year":"2016","unstructured":"Sevigny, J. et al. Amyloid PET screening for enrichment of early-stage Alzheimer disease clinical trials: experience in a phase 1b clinical trial. Alzheimer Dis. Assoc. Disord. 30, 1\u20137 (2016).","journal-title":"Alzheimer Dis. Assoc. Disord."},{"key":"1382_CR27","doi-asserted-by":"crossref","first-page":"322","DOI":"10.1056\/NEJMoa1304839","volume":"370","author":"S Salloway","year":"2014","unstructured":"Salloway, S. et al. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer\u2019s disease. N. Engl. J. Med. 370, 322\u2013333 (2014).","journal-title":"N. Engl. J. Med."},{"key":"1382_CR28","doi-asserted-by":"crossref","first-page":"10","DOI":"10.1002\/ana.25246","volume":"84","author":"MC Power","year":"2018","unstructured":"Power, M. C. et al. Combined neuropathological pathways account for age-related risk of dementia. Ann. Neurol. 84, 10\u201322 (2018).","journal-title":"Ann. Neurol."},{"key":"1382_CR29","doi-asserted-by":"crossref","first-page":"15056","DOI":"10.1038\/nrdp.2015.56","volume":"1","author":"CL Masters","year":"2015","unstructured":"Masters, C. L. et al. Alzheimer\u2019s disease. Nat. Rev. Dis. Prim. 1, 15056 (2015).","journal-title":"Nat. Rev. Dis. Prim."},{"key":"1382_CR30","doi-asserted-by":"crossref","first-page":"724","DOI":"10.1007\/s00415-020-10162-5","volume":"268","author":"M Smedinga","year":"2021","unstructured":"Smedinga, M., Darweesh, S. K. L., Bloem, B. R., Post, B. & Richard, E. Towards early disease modification of Parkinson\u2019s disease: a review of lessons learned in the Alzheimer field. J. Neurol. 268, 724\u2013733 (2021).","journal-title":"J. Neurol."},{"key":"1382_CR31","doi-asserted-by":"crossref","first-page":"698","DOI":"10.1038\/nrd3505","volume":"10","author":"E Karran","year":"2011","unstructured":"Karran, E., Mercken, M. & De Strooper, B. The amyloid cascade hypothesis for Alzheimer\u2019s disease: an appraisal for the development of therapeutics. Nat. Rev. Drug Discov. 10, 698\u2013712 (2011).","journal-title":"Nat. Rev. Drug Discov."},{"key":"1382_CR32","doi-asserted-by":"crossref","first-page":"381","DOI":"10.1016\/j.nurt.2008.05.009","volume":"5","author":"RJ Bateman","year":"2008","unstructured":"Bateman, R. J. & Klunk, W. E. Measuring target effect of proposed disease-modifying therapies in Alzheimer\u2019s disease. Neurotherapeutics 5, 381\u2013390 (2008).","journal-title":"Neurotherapeutics"},{"key":"1382_CR33","doi-asserted-by":"crossref","first-page":"61","DOI":"10.1126\/science.abb8575","volume":"370","author":"A Sierksma","year":"2020","unstructured":"Sierksma, A., Escott-Price, V. & De Strooper, B. Translating genetic risk of Alzheimer\u2019s disease into mechanistic insight and drug targets. Science 370, 61\u201366 (2020).","journal-title":"Science"},{"key":"1382_CR34","doi-asserted-by":"crossref","first-page":"e1538","DOI":"10.1212\/WNL.0000000000010256","volume":"95","author":"LE Collij","year":"2020","unstructured":"Collij, L. E. et al. Multitracer model for staging cortical amyloid deposition using PET imaging. Neurology 95, e1538\u2013e1553 (2020).","journal-title":"Neurology"},{"key":"1382_CR35","doi-asserted-by":"crossref","unstructured":"Mattsson, N., Palmqvist, S., Stomrud, E., Vogel, J. & Hansson, O. Staging \u03b2-amyloid pathology with amyloid positron emission tomography. JAMA Neurol. 76, 1319\u20131329 (2019).","DOI":"10.1001\/jamaneurol.2019.2214"},{"key":"1382_CR36","doi-asserted-by":"crossref","DOI":"10.1038\/s41467-017-01150-x","volume":"8","author":"S Palmqvist","year":"2017","unstructured":"Palmqvist, S. et al. Earliest accumulation of \u03b2-amyloid occurs within the default-mode network and concurrently affects brain connectivity. Nat. Commun. 8, 1214 (2017).","journal-title":"Nat. Commun."},{"key":"1382_CR37","doi-asserted-by":"crossref","first-page":"669","DOI":"10.1016\/S1474-4422(12)70142-4","volume":"11","author":"CM Clark","year":"2012","unstructured":"Clark, C. M. et al. Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-\u03b2 plaques: a prospective cohort study. Lancet Neurol. 11, 669\u2013678 (2012).","journal-title":"Lancet Neurol."},{"key":"1382_CR38","doi-asserted-by":"crossref","first-page":"287","DOI":"10.1001\/jamaneurol.2014.4144","volume":"72","author":"C Curtis","year":"2015","unstructured":"Curtis, C. et al. Phase 3 trial of flutemetamol labeled with radioactive fluorine 18 imaging and neuritic plaque density. JAMA Neurol. 72, 287\u2013294 (2015).","journal-title":"JAMA Neurol."},{"key":"1382_CR39","doi-asserted-by":"crossref","first-page":"964","DOI":"10.1016\/j.jalz.2015.02.004","volume":"11","author":"O Sabri","year":"2015","unstructured":"Sabri, O. et al. Florbetaben PET imaging to detect amyloid beta plaques in Alzheimer\u2019s disease: phase 3 study. Alzheimers Dement. 11, 964\u2013974 (2015).","journal-title":"Alzheimers Dement."},{"key":"1382_CR40","doi-asserted-by":"crossref","first-page":"2302","DOI":"10.1056\/NEJMoa0806142","volume":"360","author":"GM Savva","year":"2009","unstructured":"Savva, G. M. et al. Age, neuropathology, and dementia. N. Engl. J. Med. 360, 2302\u20132309 (2009).","journal-title":"N. Engl. J. Med."},{"key":"1382_CR41","doi-asserted-by":"crossref","first-page":"1924","DOI":"10.1001\/jama.2015.4668","volume":"313","author":"WJ Jansen","year":"2015","unstructured":"Jansen, W. J. et al. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA 313, 1924\u20131938 (2015).","journal-title":"JAMA"},{"key":"1382_CR42","doi-asserted-by":"crossref","first-page":"1114","DOI":"10.1001\/jamaneurol.2018.0894","volume":"75","author":"DA Wolk","year":"2018","unstructured":"Wolk, D. A. et al. Use of flutemetamol F 18-labeled positron emission tomography and other biomarkers to assess risk of clinical progression in patients with amnestic mild cognitive impairment. JAMA Neurol. 75, 1114\u20131123 (2018).","journal-title":"JAMA Neurol."},{"key":"1382_CR43","doi-asserted-by":"crossref","first-page":"2305","DOI":"10.1001\/jama.2017.6669","volume":"317","author":"MC Donohue","year":"2017","unstructured":"Donohue, M. C. et al. Association between elevated brain amyloid and subsequent cognitive decline among cognitively normal persons. JAMA 317, 2305\u20132316 (2017).","journal-title":"JAMA"},{"key":"1382_CR44","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/j.jalz.2013.01.002","volume":"9","author":"KA Johnson","year":"2013","unstructured":"Johnson, K. A. et al. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer\u2019s Association. Alzheimers Dement. 9, E1\u2013E16 (2013).","journal-title":"Alzheimers Dement."},{"key":"1382_CR45","doi-asserted-by":"crossref","first-page":"1286","DOI":"10.1001\/jama.2019.2000","volume":"321","author":"GD Rabinovici","year":"2019","unstructured":"Rabinovici, G. D. et al. Association of amyloid positron emission tomography with subsequent change in clinical management among medicare beneficiaries with mild cognitive impairment or dementia. JAMA 321, 1286\u20131294 (2019).","journal-title":"JAMA"},{"key":"1382_CR46","doi-asserted-by":"crossref","first-page":"673","DOI":"10.1016\/S1474-4422(16)00070-3","volume":"15","author":"B Olsson","year":"2016","unstructured":"Olsson, B. et al. CSF and blood biomarkers for the diagnosis of Alzheimer\u2019s disease: a systematic review and meta-analysis. Lancet Neurol. 15, 673\u2013684 (2016).","journal-title":"Lancet Neurol."},{"key":"1382_CR47","doi-asserted-by":"crossref","first-page":"1226","DOI":"10.1093\/brain\/aww015","volume":"139","author":"S Palmqvist","year":"2016","unstructured":"Palmqvist, S., Mattsson, N., Hansson, O. & Alzheimer\u2019s Disease Neuroimaging, I. Cerebrospinal fluid analysis detects cerebral amyloid-\u03b2 accumulation earlier than positron emission tomography. Brain 139, 1226\u20131236 (2016).","journal-title":"Brain"},{"key":"1382_CR48","doi-asserted-by":"crossref","first-page":"34","DOI":"10.1186\/s13195-019-0485-0","volume":"11","author":"O Hansson","year":"2019","unstructured":"Hansson, O., Lehmann, S., Otto, M., Zetterberg, H. & Lewczuk, P. Advantages and disadvantages of the use of the CSF Amyloid \u03b2 (A\u03b2) 42\/40 ratio in the diagnosis of Alzheimer\u2019s disease. Alzheimers Res. Ther. 11, 34 (2019).","journal-title":"Alzheimers Res. Ther."},{"key":"1382_CR49","doi-asserted-by":"crossref","first-page":"196","DOI":"10.1016\/j.neurobiolaging.2016.02.034","volume":"52","author":"N Mattsson","year":"2017","unstructured":"Mattsson, N. et al. Clinical validity of cerebrospinal fluid A\u03b242, tau, and phospho-tau as biomarkers for Alzheimer\u2019s disease in the context of a structured 5-phase development framework. Neurobiol. Aging 52, 196\u2013213 (2017).","journal-title":"Neurobiol. Aging"},{"key":"1382_CR50","doi-asserted-by":"crossref","first-page":"144","DOI":"10.1002\/alz.12000","volume":"16","author":"J Kaplow","year":"2020","unstructured":"Kaplow, J. et al. Concordance of Lumipulse cerebrospinal fluid t-tau\/A\u03b242 ratio with amyloid PET status. Alzheimers Dement. 16, 144\u2013152 (2020).","journal-title":"Alzheimers Dement."},{"key":"1382_CR51","doi-asserted-by":"crossref","first-page":"1470","DOI":"10.1016\/j.jalz.2018.01.010","volume":"14","author":"O Hansson","year":"2018","unstructured":"Hansson, O. et al. CSF biomarkers of Alzheimer\u2019s disease concord with amyloid-\u03b2 PET and predict clinical progression: a study of fully automated immunoassays in BioFINDER and ADNI cohorts. Alzheimers Dement. 14, 1470\u20131481 (2018).","journal-title":"Alzheimers Dement."},{"key":"1382_CR52","doi-asserted-by":"crossref","first-page":"27","DOI":"10.1016\/j.cca.2016.05.014","volume":"467","author":"J Kuhlmann","year":"2017","unstructured":"Kuhlmann, J. et al. CSF A\u03b21\u201342 \u2013 an excellent but complicated Alzheimer\u2019s biomarker \u2013 a route to standardisation. Clin. Chim. Acta 467, 27\u201333 (2017).","journal-title":"Clin. Chim. Acta"},{"key":"1382_CR53","doi-asserted-by":"publisher","DOI":"10.1002\/alz.12316","author":"O Hansson","year":"2021","unstructured":"Hansson, O. et al. The Alzheimer\u2019s Association international guidelines for handling of cerebrospinal fluid for routine clinical measurements of amyloid \u03b2 and tau. Alzheimers Dement. https:\/\/doi.org\/10.1002\/alz.12316 (2021).","journal-title":"Alzheimers Dement."},{"key":"1382_CR54","doi-asserted-by":"crossref","first-page":"1505","DOI":"10.1016\/j.jalz.2018.07.220","volume":"14","author":"LM Shaw","year":"2018","unstructured":"Shaw, L. M. et al. Appropriate use criteria for lumbar puncture and cerebrospinal fluid testing in the diagnosis of Alzheimer\u2019s disease. Alzheimers Dement 14, 1505\u20131521 (2018).","journal-title":"Alzheimers Dement"},{"key":"1382_CR55","doi-asserted-by":"crossref","DOI":"10.1038\/srep26801","volume":"6","author":"S Janelidze","year":"2016","unstructured":"Janelidze, S. et al. Plasma \u03b2-amyloid in Alzheimer\u2019s disease and vascular disease. Sci. Rep. 6, 26801 (2016).","journal-title":"Sci. Rep."},{"key":"1382_CR56","doi-asserted-by":"crossref","first-page":"841","DOI":"10.1016\/j.jalz.2017.06.2266","volume":"13","author":"V Ovod","year":"2017","unstructured":"Ovod, V. et al. Amyloid \u03b2 concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis. Alzheimers Dement. 13, 841\u2013849 (2017).","journal-title":"Alzheimers Dement."},{"key":"1382_CR57","doi-asserted-by":"crossref","first-page":"e1647","DOI":"10.1212\/WNL.0000000000008081","volume":"93","author":"SE Schindler","year":"2019","unstructured":"Schindler, S. E. et al. High-precision plasma \u03b2-amyloid 42\/40 predicts current and future brain amyloidosis. Neurology 93, e1647\u2013e1659 (2019).","journal-title":"Neurology"},{"key":"1382_CR58","doi-asserted-by":"crossref","first-page":"249","DOI":"10.1038\/nature25456","volume":"554","author":"A Nakamura","year":"2018","unstructured":"Nakamura, A. et al. High performance plasma amyloid-\u03b2 biomarkers for Alzheimer\u2019s disease. Nature 554, 249\u2013254 (2018).","journal-title":"Nature"},{"key":"1382_CR59","doi-asserted-by":"crossref","unstructured":"Palmqvist, S. et al. Performance of fully automated plasma assays as screening tests for Alzheimer disease-related \u03b2-amyloid status. JAMA Neurol. 76, 1060\u20131069 (2019).","DOI":"10.1001\/jamaneurol.2019.1632"},{"key":"1382_CR60","doi-asserted-by":"crossref","first-page":"648","DOI":"10.1002\/ana.25334","volume":"84","author":"IMW Verberk","year":"2018","unstructured":"Verberk, I. M. W. et al. Plasma amyloid as prescreener for the earliest Alzheimer pathological changes. Ann. Neurol. 84, 648\u2013658 (2018).","journal-title":"Ann. Neurol."},{"key":"1382_CR61","doi-asserted-by":"crossref","first-page":"118","DOI":"10.1186\/s13195-020-00682-7","volume":"12","author":"IMW Verberk","year":"2020","unstructured":"Verberk, I. M. W. et al. Combination of plasma amyloid beta(1-42\/1-40) and glial fibrillary acidic protein strongly associates with cerebral amyloid pathology. Alzheimers Res. Ther. 12, 118 (2020).","journal-title":"Alzheimers Res. Ther."},{"key":"1382_CR62","unstructured":"Janelidze, S. et al. Detecting amyloid positivity in early Alzheimer\u2019s disease using combinations of plasma A\u03b242\/A\u03b240 and P-tau. Alzheimers Dement. (in the press)."},{"key":"1382_CR63","doi-asserted-by":"crossref","first-page":"18","DOI":"10.1016\/j.mcn.2018.12.001","volume":"97","author":"M Scholl","year":"2019","unstructured":"Scholl, M. et al. Biomarkers for tau pathology. Mol. Cell Neurosci. 97, 18\u201333 (2019).","journal-title":"Mol. Cell Neurosci."},{"key":"1382_CR64","doi-asserted-by":"crossref","DOI":"10.1186\/s13550-020-00653-x","volume":"10","author":"MJ Pontecorvo","year":"2020","unstructured":"Pontecorvo, M. J. et al. Comparison of regional flortaucipir PET with quantitative tau immunohistochemistry in three subjects with Alzheimer\u2019s disease pathology: a clinicopathological study. EJNMMI Res. 10, 65 (2020).","journal-title":"EJNMMI Res."},{"key":"1382_CR65","doi-asserted-by":"crossref","first-page":"310","DOI":"10.1001\/jamaneurol.2018.3692","volume":"76","author":"R Smith","year":"2019","unstructured":"Smith, R., Wibom, M., Pawlik, D., Englund, E. & Hansson, O. Correlation of in vivo [18F]flortaucipir with postmortem Alzheimer disease tau pathology. JAMA Neurol. 76, 310\u2013317 (2019).","journal-title":"JAMA Neurol."},{"key":"1382_CR66","doi-asserted-by":"crossref","first-page":"3477","DOI":"10.1093\/brain\/awaa276","volume":"143","author":"DN Soleimani-Meigooni","year":"2020","unstructured":"Soleimani-Meigooni, D. N. et al. 18F-flortaucipir PET to autopsy comparisons in Alzheimer\u2019s disease and other neurodegenerative diseases. Brain 143, 3477\u20133494 (2020).","journal-title":"Brain"},{"key":"1382_CR67","doi-asserted-by":"crossref","unstructured":"Fleisher, A. S. et al. Positron emission tomography imaging with [18F]flortaucipir and postmortem assessment of Alzheimer disease neuropathologic changes. JAMA Neurol. 77, 829\u2013839 (2020).","DOI":"10.1001\/jamaneurol.2020.0528"},{"key":"1382_CR68","doi-asserted-by":"crossref","unstructured":"Leuzy, A. et al. Diagnostic performance of RO948 F 18 tau positron emission tomography in the differentiation of Alzheimer disease from other neurodegenerative disorders. JAMA Neurol. 77, 955\u2013965 (2020).","DOI":"10.1001\/jamaneurol.2020.0989"},{"key":"1382_CR69","doi-asserted-by":"crossref","first-page":"1151","DOI":"10.1001\/jama.2018.12917","volume":"320","author":"R Ossenkoppele","year":"2018","unstructured":"Ossenkoppele, R. et al. Discriminative accuracy of [18F]flortaucipir positron emission tomography for Alzheimer disease vs other neurodegenerative disorders. JAMA 320, 1151\u20131162 (2018).","journal-title":"JAMA"},{"key":"1382_CR70","doi-asserted-by":"crossref","first-page":"3286","DOI":"10.1093\/brain\/awx243","volume":"140","author":"A Bejanin","year":"2017","unstructured":"Bejanin, A. et al. Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer\u2019s disease. Brain 140, 3286\u20133300 (2017).","journal-title":"Brain"},{"key":"1382_CR71","doi-asserted-by":"crossref","first-page":"e601","DOI":"10.1212\/WNL.0000000000006875","volume":"92","author":"R Ossenkoppele","year":"2019","unstructured":"Ossenkoppele, R. et al. Associations between tau, A\u03b2, and cortical thickness with cognition in Alzheimer disease. Neurology 92, e601\u2013e612 (2019).","journal-title":"Neurology"},{"key":"1382_CR72","doi-asserted-by":"crossref","first-page":"530","DOI":"10.1523\/JNEUROSCI.2028-17.2017","volume":"38","author":"A Maass","year":"2018","unstructured":"Maass, A. et al. Entorhinal tau pathology, episodic memory decline, and neurodegeneration in aging. J. Neurosci. 38, 530\u2013543 (2018).","journal-title":"J. Neurosci."},{"key":"1382_CR73","doi-asserted-by":"crossref","first-page":"110","DOI":"10.1002\/ana.24546","volume":"79","author":"KA Johnson","year":"2016","unstructured":"Johnson, K. A. et al. Tau positron emission tomographic imaging in aging and early Alzheimer disease. Ann. Neurol. 79, 110\u2013119 (2016).","journal-title":"Ann. Neurol."},{"key":"1382_CR74","doi-asserted-by":"crossref","first-page":"3136","DOI":"10.1093\/brain\/awaa248","volume":"143","author":"CR Jack","year":"2020","unstructured":"Jack, C. R. et al. Predicting future rates of tau accumulation on PET. Brain 143, 3136\u20133150 (2020).","journal-title":"Brain"},{"key":"1382_CR75","doi-asserted-by":"crossref","unstructured":"La Joie, R. et al. Prospective longitudinal atrophy in Alzheimer\u2019s disease correlates with the intensity and topography of baseline tau-PET. Sci. Transl. Med. 12, eaau5732 (2020).","DOI":"10.1126\/scitranslmed.aau5732"},{"key":"1382_CR76","doi-asserted-by":"crossref","first-page":"1723","DOI":"10.1093\/brain\/awz090","volume":"142","author":"MJ Pontecorvo","year":"2019","unstructured":"Pontecorvo, M. J. et al. A multicentre longitudinal study of flortaucipir (18F) in normal ageing, mild cognitive impairment and Alzheimer\u2019s disease dementia. Brain 142, 1723\u20131735 (2019).","journal-title":"Brain"},{"key":"1382_CR77","doi-asserted-by":"crossref","first-page":"181","DOI":"10.1002\/ana.25395","volume":"85","author":"RA Sperling","year":"2019","unstructured":"Sperling, R. A. et al. The impact of amyloid-\u03b2 and tau on prospective cognitive decline in older individuals. Ann. Neurol. 85, 181\u2013193 (2019).","journal-title":"Ann. Neurol."},{"key":"1382_CR78","doi-asserted-by":"publisher","unstructured":"Ossenkoppele, R. et al. Tau positron emission tomography as a prognostic marker in preclinical and prodromal Alzheimer disease. JAMA Neurol. https:\/\/doi.org\/10.1001\/jamaneurol.2021.1858 (2021).","DOI":"10.1001\/jamaneurol.2021.1858"},{"key":"1382_CR79","doi-asserted-by":"crossref","first-page":"247","DOI":"10.1002\/ana.24711","volume":"80","author":"H Cho","year":"2016","unstructured":"Cho, H. et al. In vivo cortical spreading pattern of tau and amyloid in the Alzheimer disease spectrum. Ann. Neurol. 80, 247\u2013258 (2016).","journal-title":"Ann. Neurol."},{"key":"1382_CR80","volume":"11","author":"JW Vogel","year":"2020","unstructured":"Vogel, J. W. et al. Spread of pathological tau proteins through communicating neurons in human Alzheimer\u2019s disease. Nat. Commun. 11, 2612 (2020).","journal-title":"Nat. Commun."},{"key":"1382_CR81","doi-asserted-by":"crossref","first-page":"2818","DOI":"10.1093\/brain\/awaa180","volume":"143","author":"TA Pascoal","year":"2020","unstructured":"Pascoal, T. A. et al. 18F-MK-6240 PET for early and late detection of neurofibrillary tangles. Brain 143, 2818\u20132830 (2020).","journal-title":"Brain"},{"key":"1382_CR82","doi-asserted-by":"crossref","unstructured":"Sanchez, J. S. et al. The cortical origin and initial spread of medial temporal tauopathy in Alzheimer\u2019s disease assessed with positron emission tomography. Sci. Transl. Med. 13, eabc0655 (2021).","DOI":"10.1126\/scitranslmed.abc0655"},{"key":"1382_CR83","doi-asserted-by":"crossref","first-page":"1551","DOI":"10.1093\/brain\/aww027","volume":"139","author":"R Ossenkoppele","year":"2016","unstructured":"Ossenkoppele, R. et al. Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer\u2019s disease. Brain 139, 1551\u20131567 (2016).","journal-title":"Brain"},{"key":"1382_CR84","doi-asserted-by":"publisher","unstructured":"Vogel, J. W. et al. Four distinct trajectories of tau deposition identified in Alzheimer\u2019s disease. Nat. Med. https:\/\/doi.org\/10.1038\/s41591-021-01309-6 (2021).","DOI":"10.1038\/s41591-021-01309-6"},{"key":"1382_CR85","doi-asserted-by":"crossref","DOI":"10.1038\/s41467-019-14159-1","volume":"11","author":"N Franzmeier","year":"2020","unstructured":"Franzmeier, N. et al. Functional brain architecture is associated with the rate of tau accumulation in Alzheimer\u2019s disease. Nat. Commun. 11, 347 (2020).","journal-title":"Nat. Commun."},{"key":"1382_CR86","doi-asserted-by":"crossref","first-page":"424","DOI":"10.1038\/s41593-018-0070-z","volume":"21","author":"HIL Jacobs","year":"2018","unstructured":"Jacobs, H. I. L. et al. Structural tract alterations predict downstream tau accumulation in amyloid-positive older individuals. Nat. Neurosci. 21, 424\u2013431 (2018).","journal-title":"Nat. Neurosci."},{"key":"1382_CR87","doi-asserted-by":"crossref","first-page":"1517","DOI":"10.1093\/brain\/awy059","volume":"141","author":"CR Jack Jr.","year":"2018","unstructured":"Jack, C. R. Jr. et al. Longitudinal tau PET in ageing and Alzheimer\u2019s disease. Brain 141, 1517\u20131528 (2018).","journal-title":"Brain"},{"key":"1382_CR88","doi-asserted-by":"crossref","first-page":"3805","DOI":"10.1093\/brain\/awaa327","volume":"143","author":"R Smith","year":"2020","unstructured":"Smith, R. et al. The accumulation rate of tau aggregates is higher in females and younger amyloid-positive subjects. Brain 143, 3805\u20133815 (2020).","journal-title":"Brain"},{"key":"1382_CR89","doi-asserted-by":"crossref","first-page":"643","DOI":"10.1111\/joim.12816","volume":"284","author":"K Blennow","year":"2018","unstructured":"Blennow, K. & Zetterberg, H. Biomarkers for Alzheimer\u2019s disease: current status and prospects for the future. J. Intern. Med. 284, 643\u2013663 (2018).","journal-title":"J. Intern. Med."},{"key":"1382_CR90","doi-asserted-by":"crossref","DOI":"10.1038\/s41598-019-54204-z","volume":"9","author":"K Blennow","year":"2019","unstructured":"Blennow, K. et al. Predicting clinical decline and conversion to Alzheimer\u2019s disease or dementia using novel Elecsys A\u03b2(1\u201342), pTau and tTau CSF immunoassays. Sci. Rep. 9, 19024 (2019).","journal-title":"Sci. Rep."},{"key":"1382_CR91","doi-asserted-by":"crossref","DOI":"10.1038\/s41467-020-15436-0","volume":"11","author":"S Janelidze","year":"2020","unstructured":"Janelidze, S. et al. Cerebrospinal fluid p-tau217 performs better than p-tau181 as a biomarker of Alzheimer\u2019s disease. Nat. Commun. 11, 1683 (2020).","journal-title":"Nat. Commun."},{"key":"1382_CR92","doi-asserted-by":"crossref","first-page":"e3026","DOI":"10.1212\/WNL.0000000000010814","volume":"95","author":"J Hanes","year":"2020","unstructured":"Hanes, J. et al. Evaluation of a novel immunoassay to detect p-tau Thr217 in the CSF to distinguish Alzheimer disease from other dementias. Neurology 95, e3026\u2013e3035 (2020).","journal-title":"Neurology"},{"key":"1382_CR93","doi-asserted-by":"crossref","unstructured":"Horie, K., Barthelemy, N. R., Sato, C. & Bateman, R. J. CSF tau microtubule binding region identifies tau tangle and clinical stages of Alzheimer\u2019s disease. Brain 144, 515\u2013527 (2020).","DOI":"10.1093\/brain\/awaa373"},{"key":"1382_CR94","doi-asserted-by":"crossref","first-page":"650","DOI":"10.1093\/brain\/awz346","volume":"143","author":"K Blennow","year":"2020","unstructured":"Blennow, K. et al. Cerebrospinal fluid tau fragment correlates with tau PET: a candidate biomarker for tangle pathology. Brain 143, 650\u2013660 (2020).","journal-title":"Brain"},{"key":"1382_CR95","doi-asserted-by":"crossref","first-page":"379","DOI":"10.1038\/s41591-020-0755-1","volume":"26","author":"S Janelidze","year":"2020","unstructured":"Janelidze, S. et al. Plasma P-tau181 in Alzheimer\u2019s disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer\u2019s dementia. Nat. Med. 26, 379\u2013386 (2020).","journal-title":"Nat. Med."},{"key":"1382_CR96","doi-asserted-by":"crossref","first-page":"267","DOI":"10.1007\/s00401-020-02195-x","volume":"140","author":"J Lantero Rodriguez","year":"2020","unstructured":"Lantero Rodriguez, J. et al. Plasma p-tau181 accurately predicts Alzheimer\u2019s disease pathology at least 8 years prior to post-mortem and improves the clinical characterisation of cognitive decline. Acta Neuropathol. 140, 267\u2013278 (2020).","journal-title":"Acta Neuropathol."},{"key":"1382_CR97","doi-asserted-by":"crossref","first-page":"772","DOI":"10.1001\/jama.2020.12134","volume":"324","author":"S Palmqvist","year":"2020","unstructured":"Palmqvist, S. et al. Discriminative accuracy of plasma phospho-tau217 for Alzheimer disease vs other neurodegenerative disorders. JAMA 324, 772\u2013781 (2020).","journal-title":"JAMA"},{"key":"1382_CR98","doi-asserted-by":"crossref","first-page":"387","DOI":"10.1038\/s41591-020-0762-2","volume":"26","author":"EH Thijssen","year":"2020","unstructured":"Thijssen, E. H. et al. Diagnostic value of plasma phosphorylated tau181 in Alzheimer\u2019s disease and frontotemporal lobar degeneration. Nat. Med. 26, 387\u2013397 (2020).","journal-title":"Nat. Med."},{"key":"1382_CR99","doi-asserted-by":"crossref","first-page":"422","DOI":"10.1016\/S1474-4422(20)30071-5","volume":"19","author":"TK Karikari","year":"2020","unstructured":"Karikari, T. K. et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer\u2019s disease: a diagnostic performance and prediction modelling study using data from four prospective cohorts. Lancet Neurol. 19, 422\u2013433 (2020).","journal-title":"Lancet Neurol."},{"key":"1382_CR100","doi-asserted-by":"crossref","unstructured":"Karikari, T. K. et al. Diagnostic performance and prediction of clinical progression of plasma phospho-tau181 in the Alzheimer\u2019s Disease Neuroimaging Initiative. Mol. Psychiatry 26, 429\u2013442 (2021).","DOI":"10.1038\/s41380-020-00923-z"},{"key":"1382_CR101","doi-asserted-by":"crossref","first-page":"114","DOI":"10.1038\/s43587-020-00003-5","volume":"1","author":"N Cullen","year":"2021","unstructured":"Cullen, N. et al. Individualized prognosis of cognitive decline and dementia in mild cognitive impairment based on plasma biomarker combinations. Nat. Aging 1, 114\u2013123 (2021).","journal-title":"Nat. Aging"},{"key":"1382_CR102","doi-asserted-by":"crossref","unstructured":"Cullen, N. C. et al. Plasma biomarkers of Alzheimer\u2019s disease predict cognitive decline and could improve clinical trials in the cognitively unimpaired elderly (submitted, 2021).","DOI":"10.1101\/2021.01.22.21250293"},{"key":"1382_CR103","doi-asserted-by":"crossref","first-page":"3234","DOI":"10.1093\/brain\/awaa286","volume":"143","author":"N Mattsson-Carlgren","year":"2020","unstructured":"Mattsson-Carlgren, N. et al. Longitudinal plasma p-tau217 is increased in early stages of Alzheimer\u2019s disease. Brain 143, 3234\u20133241 (2020).","journal-title":"Brain"},{"key":"1382_CR104","doi-asserted-by":"publisher","unstructured":"Mattsson-Carlgren, N. et al. Soluble P-tau217 reflects amyloid and tau pathology and mediates the association of amyloid with tau. EMBO Mol. Med. https:\/\/doi.org\/10.15252\/emmm.202114022 (2021).","DOI":"10.15252\/emmm.202114022"},{"key":"1382_CR105","doi-asserted-by":"publisher","unstructured":"O\u2019Connor, A. et al. Plasma phospho-tau181 in presymptomatic and symptomatic familial Alzheimer\u2019s disease: a longitudinal cohort study. Mol. Psychiatry https:\/\/doi.org\/10.1038\/s41380-020-0838-x (2020).","DOI":"10.1038\/s41380-020-0838-x"},{"key":"1382_CR106","doi-asserted-by":"crossref","first-page":"e11170","DOI":"10.15252\/emmm.201911170","volume":"11","author":"S Palmqvist","year":"2019","unstructured":"Palmqvist, S. et al. Cerebrospinal fluid and plasma biomarker trajectories with increasing amyloid deposition in Alzheimer\u2019s disease. EMBO Mol. Med. 11, e11170 (2019).","journal-title":"EMBO Mol. Med."},{"key":"1382_CR107","doi-asserted-by":"crossref","unstructured":"Janelidze, S. et al. Associations of plasma phospho-tau217 levels with tau positron emission tomography in early Alzheimer disease. JAMA Neurol. 78, 149\u2013156 (2020).","DOI":"10.1001\/jamaneurol.2020.4201"},{"key":"1382_CR108","doi-asserted-by":"crossref","first-page":"398","DOI":"10.1038\/s41591-020-0781-z","volume":"26","author":"NR Barthelemy","year":"2020","unstructured":"Barthelemy, N. R. et al. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer\u2019s disease. Nat. Med. 26, 398\u2013407 (2020).","journal-title":"Nat. Med."},{"key":"1382_CR109","doi-asserted-by":"crossref","first-page":"eaaz2387","DOI":"10.1126\/sciadv.aaz2387","volume":"6","author":"N Mattsson-Carlgren","year":"2020","unstructured":"Mattsson-Carlgren, N. et al. Abeta deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer\u2019s disease. Sci. Adv. 6, eaaz2387 (2020).","journal-title":"Sci. Adv."},{"key":"1382_CR110","doi-asserted-by":"crossref","first-page":"861","DOI":"10.1016\/j.neuron.2018.04.035","volume":"98","author":"C Sato","year":"2018","unstructured":"Sato, C. et al. Tau kinetics in neurons and the human central nervous system. Neuron 98, 861\u2013864 (2018).","journal-title":"Neuron"},{"key":"1382_CR111","doi-asserted-by":"crossref","first-page":"573","DOI":"10.1016\/S1474-4422(19)30024-9","volume":"18","author":"L Parnetti","year":"2019","unstructured":"Parnetti, L. et al. CSF and blood biomarkers for Parkinson\u2019s disease. Lancet Neurol. 18, 573\u2013586 (2019).","journal-title":"Lancet Neurol."},{"key":"1382_CR112","doi-asserted-by":"crossref","first-page":"812","DOI":"10.1002\/acn3.338","volume":"3","author":"G Fairfoul","year":"2016","unstructured":"Fairfoul, G. et al. Alpha-synuclein RT-QuIC in the CSF of patients with alpha-synucleinopathies. Ann. Clin. Transl. Neurol. 3, 812\u2013818 (2016).","journal-title":"Ann. Clin. Transl. Neurol."},{"key":"1382_CR113","doi-asserted-by":"crossref","first-page":"49","DOI":"10.1007\/s00401-020-02160-8","volume":"140","author":"M Rossi","year":"2020","unstructured":"Rossi, M. et al. Ultrasensitive RT-QuIC assay with high sensitivity and specificity for Lewy body-associated synucleinopathies. Acta Neuropathol. 140, 49\u201362 (2020).","journal-title":"Acta Neuropathol."},{"key":"1382_CR114","doi-asserted-by":"crossref","first-page":"536","DOI":"10.1002\/mds.27646","volume":"34","author":"UJ Kang","year":"2019","unstructured":"Kang, U. J. et al. Comparative study of cerebrospinal fluid \u03b1-synuclein seeding aggregation assays for diagnosis of Parkinson\u2019s disease. Mov. Disord. 34, 536\u2013544 (2019).","journal-title":"Mov. Disord."},{"key":"1382_CR115","doi-asserted-by":"crossref","first-page":"503","DOI":"10.1002\/ana.25824","volume":"88","author":"W Singer","year":"2020","unstructured":"Singer, W. et al. Alpha-synuclein oligomers and neurofilament light chain in spinal fluid differentiate multiple system atrophy from Lewy body synucleinopathies. Ann. Neurol. 88, 503\u2013512 (2020).","journal-title":"Ann. Neurol."},{"key":"1382_CR116","doi-asserted-by":"crossref","first-page":"273","DOI":"10.1038\/s41586-020-1984-7","volume":"578","author":"M Shahnawaz","year":"2020","unstructured":"Shahnawaz, M. et al. Discriminating \u03b1-synuclein strains in Parkinson\u2019s disease and multiple system atrophy. Nature 578, 273\u2013277 (2020).","journal-title":"Nature"},{"key":"1382_CR117","doi-asserted-by":"crossref","unstructured":"Wang, Z. et al. Skin \u03b1-synuclein aggregation seeding activity as a novel biomarker for Parkinson disease. JAMA Neurol. 78, 1\u201311 (2020).","DOI":"10.1001\/jamaneurol.2020.3311"},{"key":"1382_CR118","doi-asserted-by":"crossref","first-page":"2230","DOI":"10.1002\/mds.28242","volume":"35","author":"S Manne","year":"2020","unstructured":"Manne, S. et al. Blinded RT-QuIC analysis of alpha-synuclein biomarker in skin tissue from Parkinson\u2019s disease patients. Mov. Disord. 35, 2230\u20132239 (2020).","journal-title":"Mov. Disord."},{"key":"1382_CR119","doi-asserted-by":"crossref","first-page":"1661","DOI":"10.1002\/acn3.51158","volume":"7","author":"NC Cullen","year":"2020","unstructured":"Cullen, N. C. et al. Comparing progression biomarkers in clinical trials of early Alzheimer\u2019s disease. Ann. Clin. Transl. Neurol. 7, 1661\u20131673 (2020).","journal-title":"Ann. Clin. Transl. Neurol."},{"key":"1382_CR120","doi-asserted-by":"crossref","first-page":"596","DOI":"10.2967\/jnumed.108.059998","volume":"51","author":"DJ Brooks","year":"2010","unstructured":"Brooks, D. J. Imaging approaches to Parkinson disease. J. Nucl. Med. 51, 596\u2013609 (2010).","journal-title":"J. Nucl. Med."},{"key":"1382_CR121","doi-asserted-by":"crossref","first-page":"329","DOI":"10.1002\/ana.25682","volume":"87","author":"D Matuskey","year":"2020","unstructured":"Matuskey, D. et al. Synaptic changes in Parkinson disease assessed with in vivo imaging. Ann. Neurol. 87, 329\u2013338 (2020).","journal-title":"Ann. Neurol."},{"key":"1382_CR122","doi-asserted-by":"crossref","first-page":"974","DOI":"10.1002\/alz.12097","volume":"16","author":"AP Mecca","year":"2020","unstructured":"Mecca, A. P. et al. In vivo measurement of widespread synaptic loss in Alzheimer\u2019s disease with SV2A PET. Alzheimers Dement. 16, 974\u2013982 (2020).","journal-title":"Alzheimers Dement."},{"key":"1382_CR123","doi-asserted-by":"publisher","unstructured":"Chen, M. K. et al. Comparison of [11C]UCB-J and [18F]FDG PET in Alzheimer\u2019s disease: a tracer kinetic modeling study. J. Cereb. Blood Flow Metab. https:\/\/doi.org\/10.1177\/0271678X211004312 (2021).","DOI":"10.1177\/0271678X211004312"},{"key":"1382_CR124","doi-asserted-by":"crossref","first-page":"951","DOI":"10.1016\/S1474-4422(20)30314-8","volume":"19","author":"G Chetelat","year":"2020","unstructured":"Chetelat, G. et al. Amyloid-PET and 18F-FDG-PET in the diagnostic investigation of Alzheimer\u2019s disease and other dementias. Lancet Neurol. 19, 951\u2013962 (2020).","journal-title":"Lancet Neurol."},{"key":"1382_CR125","doi-asserted-by":"crossref","first-page":"577","DOI":"10.1038\/s41582-018-0058-z","volume":"14","author":"M Khalil","year":"2018","unstructured":"Khalil, M. et al. Neurofilaments as biomarkers in neurological disorders. Nat. Rev. Neurol. 14, 577\u2013589 (2018).","journal-title":"Nat. Rev. Neurol."},{"key":"1382_CR126","doi-asserted-by":"publisher","unstructured":"Ashton, N. et al. A multicentre validation study of the diagnostic value of plasma neurofilament light. Nat. Commun. https:\/\/doi.org\/10.1038\/s41467-021-23620-z (2021).","DOI":"10.1038\/s41467-021-23620-z"},{"key":"1382_CR127","doi-asserted-by":"crossref","first-page":"277","DOI":"10.1038\/s41591-018-0304-3","volume":"25","author":"O Preische","year":"2019","unstructured":"Preische, O. et al. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer\u2019s disease. Nat. Med. 25, 277\u2013283 (2019).","journal-title":"Nat. Med."},{"key":"1382_CR128","doi-asserted-by":"crossref","first-page":"e1201","DOI":"10.1212\/WNL.0000000000009097","volume":"94","author":"B Delcoigne","year":"2020","unstructured":"Delcoigne, B. et al. Blood neurofilament light levels segregate treatment effects in multiple sclerosis. Neurology 94, e1201\u2013e1212 (2020).","journal-title":"Neurology"},{"key":"1382_CR129","doi-asserted-by":"crossref","first-page":"2129","DOI":"10.1007\/s00415-019-09389-8","volume":"266","author":"B Olsson","year":"2019","unstructured":"Olsson, B. et al. NFL is a marker of treatment response in children with SMA treated with nusinersen. J. Neurol. 266, 2129\u20132136 (2019).","journal-title":"J. Neurol."},{"key":"1382_CR130","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1007\/s00401-018-1851-x","volume":"136","author":"E Portelius","year":"2018","unstructured":"Portelius, E. et al. Cerebrospinal fluid neurogranin concentration in neurodegeneration: relation to clinical phenotypes and neuropathology. Acta Neuropathol. 136, 363\u2013376 (2018).","journal-title":"Acta Neuropathol."},{"key":"1382_CR131","doi-asserted-by":"crossref","first-page":"3373","DOI":"10.1093\/brain\/awv267","volume":"138","author":"E Portelius","year":"2015","unstructured":"Portelius, E. et al. Cerebrospinal fluid neurogranin: relation to cognition and neurodegeneration in Alzheimer\u2019s disease. Brain 138, 3373\u20133385 (2015).","journal-title":"Brain"},{"key":"1382_CR132","doi-asserted-by":"crossref","unstructured":"Verberk, I. M. W. et al. Serum markers glial fibrillary acidic protein and neurofilament light for prognosis and monitoring in cognitively normal older people: a prospective memory clinic-based cohort study. Lancet Healthy Longevity 2, E87\u2013E95 (2021).","DOI":"10.1016\/S2666-7568(20)30061-1"},{"key":"1382_CR133","doi-asserted-by":"crossref","first-page":"68","DOI":"10.1186\/s13195-021-00804-9","volume":"13","author":"C Cicognola","year":"2021","unstructured":"Cicognola, C. et al. Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment. Alzheimers Res. Ther. 13, 68 (2021).","journal-title":"Alzheimers Res. Ther."},{"key":"1382_CR134","doi-asserted-by":"crossref","first-page":"263","DOI":"10.1136\/jnnp-2019-321954","volume":"91","author":"C Heller","year":"2020","unstructured":"Heller, C. et al. Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia. J. Neurol. Neurosurg. Psychiatry 91, 263\u2013270 (2020).","journal-title":"J. Neurol. Neurosurg. Psychiatry"},{"key":"1382_CR135","doi-asserted-by":"crossref","first-page":"10","DOI":"10.1097\/RLI.0000000000000723","volume":"56","author":"EP Elschot","year":"2021","unstructured":"Elschot, E. P. et al. A comprehensive view on MRI techniques for imaging blood\u2013brain barrier integrity. Invest. Radio. 56, 10\u201319 (2021).","journal-title":"Invest. Radio."},{"key":"1382_CR136","doi-asserted-by":"crossref","first-page":"104","DOI":"10.1016\/j.neurobiolaging.2016.11.017","volume":"51","author":"S Janelidze","year":"2017","unstructured":"Janelidze, S. et al. Increased blood-brain barrier permeability is associated with dementia and diabetes but not amyloid pathology or APOE genotype. Neurobiol. Aging 51, 104\u2013112 (2017).","journal-title":"Neurobiol. Aging"},{"key":"1382_CR137","doi-asserted-by":"crossref","first-page":"270","DOI":"10.1038\/s41591-018-0297-y","volume":"25","author":"DA Nation","year":"2019","unstructured":"Nation, D. A. et al. Blood\u2013brain barrier breakdown is an early biomarker of human cognitive dysfunction. Nat. Med. 25, 270\u2013276 (2019).","journal-title":"Nat. Med."},{"key":"1382_CR138","doi-asserted-by":"crossref","unstructured":"Mintun, M. A. et al. Donanemab in early Alzheimer\u2019s disease. N. Engl. J. Med. 384, 1691\u20131704 (2021).","DOI":"10.1056\/NEJMoa2100708"},{"key":"1382_CR139","doi-asserted-by":"publisher","unstructured":"Palmqvist, S. et al. Prediction of future Alzheimer\u2019s disease dementia using plasma phospho-tau combined with other accessible measures. Nat. Med. https:\/\/doi.org\/10.1038\/s41591-021-01348-z (2021).","DOI":"10.1038\/s41591-021-01348-z"},{"key":"1382_CR140","doi-asserted-by":"crossref","first-page":"8667","DOI":"10.1039\/C8CC02204F","volume":"54","author":"M Tornquist","year":"2018","unstructured":"Tornquist, M. et al. Secondary nucleation in amyloid formation. Chem. Commun. 54, 8667\u20138684 (2018).","journal-title":"Chem. Commun."},{"key":"1382_CR141","doi-asserted-by":"crossref","first-page":"755","DOI":"10.1007\/s00401-014-1349-0","volume":"128","author":"JF Crary","year":"2014","unstructured":"Crary, J. F. et al. Primary age-related tauopathy (PART): a common pathology associated with human aging. Acta Neuropathol. 128, 755\u2013766 (2014).","journal-title":"Acta Neuropathol."},{"key":"1382_CR142","doi-asserted-by":"crossref","first-page":"705","DOI":"10.1007\/s00401-017-1681-2","volume":"133","author":"KA Josephs","year":"2017","unstructured":"Josephs, K. A. et al. Tau aggregation influences cognition and hippocampal atrophy in the absence of \u03b2-amyloid: a clinico-imaging-pathological study of primary age-related tauopathy (PART). Acta Neuropathol. 133, 705\u2013715 (2017).","journal-title":"Acta Neuropathol."},{"key":"1382_CR143","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1016\/j.sbi.2020.05.011","volume":"64","author":"SHW Scheres","year":"2020","unstructured":"Scheres, S. H. W., Zhang, W., Falcon, B. & Goedert, M. Cryo-EM structures of tau filaments. Curr. Opin. Struct. Biol. 64, 17\u201325 (2020).","journal-title":"Curr. Opin. Struct. Biol."},{"key":"1382_CR144","doi-asserted-by":"crossref","first-page":"13","DOI":"10.1038\/nrneurol.2012.242","volume":"9","author":"M Goedert","year":"2013","unstructured":"Goedert, M., Spillantini, M. G., Del Tredici, K. & Braak, H. 100 years of Lewy pathology. Nat. Rev. Neurol. 9, 13\u201324 (2013).","journal-title":"Nat. Rev. Neurol."},{"key":"1382_CR145","doi-asserted-by":"crossref","first-page":"1699","DOI":"10.1016\/j.cell.2020.10.029","volume":"183","author":"H Wesseling","year":"2020","unstructured":"Wesseling, H. et al. Tau PTM profiles identify patient heterogeneity and stages of Alzheimer\u2019s disease. Cell 183, 1699\u20131713 (2020).","journal-title":"Cell"},{"key":"1382_CR146","doi-asserted-by":"crossref","first-page":"S281","DOI":"10.3233\/JPD-191721","volume":"9","author":"P Borghammer","year":"2019","unstructured":"Borghammer, P. & Van Den Berge, N. Brain-first versus gut-first Parkinson\u2019s disease: a hypothesis. J. Parkinsons Dis. 9, S281\u2013S295 (2019).","journal-title":"J. Parkinsons Dis."},{"key":"1382_CR147","doi-asserted-by":"crossref","first-page":"2084","DOI":"10.1016\/S0140-6736(17)31287-4","volume":"390","author":"MA van Es","year":"2017","unstructured":"van Es, M. A. et al. Amyotrophic lateral sclerosis. Lancet 390, 2084\u20132098 (2017).","journal-title":"Lancet"},{"key":"1382_CR148","doi-asserted-by":"crossref","first-page":"1503","DOI":"10.1093\/brain\/awz099","volume":"142","author":"PT Nelson","year":"2019","unstructured":"Nelson, P. T. et al. Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report. Brain 142, 1503\u20131527 (2019).","journal-title":"Brain"}],"container-title":["Nature Medicine"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/www.nature.com\/articles\/s41591-021-01382-x.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/www.nature.com\/articles\/s41591-021-01382-x","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/www.nature.com\/articles\/s41591-021-01382-x.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,4]],"date-time":"2023-11-04T09:24:24Z","timestamp":1699089864000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.nature.com\/articles\/s41591-021-01382-x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,6]]},"references-count":148,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2021,6]]}},"alternative-id":["1382"],"URL":"https:\/\/doi.org\/10.1038\/s41591-021-01382-x","relation":{},"ISSN":["1078-8956","1546-170X"],"issn-type":[{"value":"1078-8956","type":"print"},{"value":"1546-170X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,6]]},"assertion":[{"value":"8 February 2021","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"3 May 2021","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"3 June 2021","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"O.H. acquired research support (for the institution) from AVID Radiopharmaceuticals, Biogen, Eli Lilly, Eisai, GE Healthcare, Pfizer and Roche. In the past 2 years, he has received consultancy\/speaker fees from AC Immune, Alzpath, Biogen, Cerveau and Roche.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}