P‐tau/Aβ42 and Aβ42/40 ratios in CSF are equally predictive of amyloid PET status

Measurement of amyloid beta (Aβ40 and Aβ42) and tau (phosphorylated tau [p‐tau] and total tau [t‐tau]) in cerebrospinal fluid (CSF) can be utilized to differentiate clinical and preclinical Alzheimer's disease dementia (AD) from other neurodegenerative processes.

[1]  Hans Förstl,et al.  The solely A+ CSF Aβ42/40 ratio using Elecsys® assays performs similar to A/T and A/N ratios in predicting amyloid PET positivity , 2020 .

[2]  W. M. van der Flier,et al.  Prediction of amyloid PET status using the LUMIPULSE G β‐amyloid ratio (1‐42/1‐40) , 2020 .

[3]  M. Sabbagh,et al.  Alzheimer’s Disease Drug Development Pipeline 2020 , 2020, The Journal of Prevention of Alzheimer's Disease.

[4]  C. Jack,et al.  Better stress coping associated with lower tau in amyloid-positive cognitively unimpaired older adults , 2020, Neurology.

[5]  L. Shaw,et al.  Racial Disparity in Cerebrospinal Fluid Amyloid and Tau Biomarkers and Associated Cutoffs for Mild Cognitive Impairment , 2019, JAMA network open.

[6]  I. Santana,et al.  Clinical validation of the Lumipulse G cerebrospinal fluid assays for routine diagnosis of Alzheimer’s disease , 2019, Alzheimer's Research & Therapy.

[7]  C. Jack,et al.  Comparison of variables associated with cerebrospinal fluid neurofilament, total-tau, and neurogranin , 2019, Alzheimer's & Dementia.

[8]  K. Blennow,et al.  Method comparison study of the Elecsys® β-Amyloid (1-42) CSF assay versus comparator assays and LC-MS/MS. , 2019, Clinical biochemistry.

[9]  P. Scheltens,et al.  The “rights” of precision drug development for Alzheimer’s disease , 2019, Alzheimer's Research & Therapy.

[10]  J. Clarimón,et al.  Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse , 2019, Annals of clinical and translational neurology.

[11]  S. Lehmann,et al.  Impact of CSF storage volume on the analysis of Alzheimer's disease biomarkers on an automated platform. , 2019, Clinica chimica acta; international journal of clinical chemistry.

[12]  Brian A. Gordon,et al.  Assessment of Racial Disparities in Biomarkers for Alzheimer Disease , 2019, JAMA neurology.

[13]  José Luis Molinuevo,et al.  Current state of Alzheimer’s fluid biomarkers , 2018, Acta Neuropathologica.

[14]  A. Fagan,et al.  Cerebrospinal fluid biomarkers measured by Elecsys assays compared to amyloid imaging , 2018, Alzheimer's & Dementia.

[15]  Simone Lista,et al.  Blood-based biomarkers for Alzheimer disease: mapping the road to the clinic , 2018, Nature Reviews Neurology.

[16]  C. Jack,et al.  NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease , 2018, Alzheimer's & Dementia.

[17]  J. Schott,et al.  Amyloid β peptides are differentially vulnerable to preanalytical surface exposure, an effect incompletely mitigated by the use of ratios , 2018, Alzheimer's & dementia.

[18]  J. Trojanowski,et al.  CSF biomarkers of Alzheimer’s disease concord with amyloid-β PETand predict clinical progression: A study of fully automated immunoassays in BioFINDER and ADNI cohorts , 2018, Alzheimer's & Dementia.

[19]  William T. Hu,et al.  Race modifies the relationship between cognition and Alzheimer’s disease cerebrospinal fluid biomarkers , 2017, Alzheimer's Research & Therapy.

[20]  J. Cummings,et al.  Lessons Learned from Alzheimer Disease: Clinical Trials with Negative Outcomes , 2017, Clinical and translational science.

[21]  David T. Jones,et al.  Defining imaging biomarker cut points for brain aging and Alzheimer's disease , 2017, Alzheimer's & Dementia.

[22]  K. Blennow,et al.  No diurnal variation of classical and candidate biomarkers of Alzheimer’s disease in CSF , 2016, Molecular Neurodegeneration.

[23]  K. Blennow,et al.  Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1–42) in human cerebrospinal fluid , 2016, Alzheimer's & Dementia.

[24]  K. Blennow,et al.  CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios: better diagnostic markers of Alzheimer disease , 2016, Annals of clinical and translational neurology.

[25]  K. Blennow,et al.  Accuracy of brain amyloid detection in clinical practice using cerebrospinal fluid β-amyloid 42: a cross-validation study against amyloid positron emission tomography. , 2014, JAMA neurology.

[26]  L. Ferrucci,et al.  Correspondence between in vivo 11C-PiB-PET amyloid imaging and postmortem, region-matched assessment of plaques , 2012, Acta Neuropathologica.

[27]  J. Morris,et al.  The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.

[28]  E G Tangalos,et al.  Prevalence of mild cognitive impairment is higher in men , 2010, Neurology.

[29]  Wendy R. Sanhai,et al.  Biomarkers for Alzheimer's disease: academic, industry and regulatory perspectives , 2010, Nature Reviews Drug Discovery.

[30]  Sakari Savolainen,et al.  Assessment of beta-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11-labeled Pittsburgh Compound B. , 2008, Archives of neurology.

[31]  V. Pankratz,et al.  The Mayo Clinic Study of Aging: Design and Sampling, Participation, Baseline Measures and Sample Characteristics , 2008, Neuroepidemiology.

[32]  C. Sfagos,et al.  Cerebrospinal fluid tau, phospho‐tau181 and β‐amyloid1−42 in idiopathic normal pressure hydrocephalus: a discrimination from Alzheimer's disease , 2007, European journal of neurology.

[33]  Nick C Fox,et al.  Effects of Aβ immunization (AN1792) on MRI measures of cerebral volume in Alzheimer disease , 2005, Neurology.

[34]  R. Petersen.  Mild cognitive impairment as a diagnostic entity , 2004, Journal of internal medicine.

[35]  W. Klunk,et al.  Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B , 2004, Annals of neurology.

[36]  J. Cummings.  The Role of Biomarkers in Alzheimer's Disease Drug Development. , 2019, Advances in experimental medicine and biology.

[37]  K. Blennow,et al.  Anti-Tau Trials for Alzheimer’s Disease: A Report from the EU/US/CTAD Task Force , 2019, The Journal of Prevention of Alzheimer's Disease.

[38]  C. Malaplate-Armand,et al.  Cerebrospinal Fluid Aβ42/Aβ40 as a Means to Limiting Tube- and Storage-Dependent Pre-Analytical Variability in Clinical Setting. , 2017, Journal of Alzheimer's disease : JAD.

[39]  G. Magnani,et al.  Cerebrospinal Fluid Amyloid-β 42, Total Tau and Phosphorylated Tau are Low in Patients with Normal Pressure Hydrocephalus: Analogies and Differences with Alzheimer's Disease. , 2017, Journal of Alzheimer's disease : JAD.

[40]  L. Parnetti,et al.  Cerebrospinal Fluid Biomarkers for Target Engagement and Efficacy in Clinical Trials for Alzheimer's and Parkinson's Diseases. , 2016, Frontiers of neurology and neuroscience.

[41]  D. Selkoe.  Alzheimer's disease. , 2011, Cold Spring Harbor perspectives in biology.

[42]  F. Jessen,et al.  Amyloid beta peptide ratio 42/40 but not A beta 42 correlates with phospho-Tau in patients with low- and high-CSF A beta 40 load. , 2007, Journal of neurochemistry.