Cerebrospinal Fluid Biomarker Signature in Alzheimer’s Disease Neuroimaging Initiative Subjects
By Leslie M. Shaw, H. Vanderstichele, M. Knapik-Czajka, Christopher M. Clark, P. Aisen, R. Petersen, Kaj Blennow, Holly D. Soares, A. Simon, P. Lewczuk and 5 more. Annals of Neurology, 2009
2,163 citations recorded by the source corpus.
Develop a cerebrospinal fluid biomarker signature for mild Alzheimer's disease (AD) in Alzheimer's Disease Neuroimaging Initiative (ADNI) subjects.
Subfields: Molecular Biology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/365bc7651a03fa1c1c02dbd72d800a1d97855484
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In Molecular Biology
- William W. Seeley
- Oskar Hansson
- Dinggang Shen
- Henrik Zetterberg
- Reisa A. Sperling
- Suzanne L. Baker
- John Q. Trojanowski
- William J. Jagust
In Physiology
- Kaj Blennow
- Clifford R. Jack Jr.
- Henrik Zetterberg
- Oskar Hansson
- Richard P. Mayeux
- Reisa A. Sperling
- Yaakov Stern
- William W. Seeley
In Psychiatry and Mental health
- Dinggang Shen
- Clifford R. Jack Jr.
- Daoqiang Zhang
- Henrik Zetterberg
- Kaj Blennow
- Oskar Hansson
- Richard P. Mayeux
- Reisa A. Sperling
Citations in the corpus
- Sex Modifies the APOE-Related Risk of Developing Alzheimer's Disease (2014, neutral): “Biomarkers were assessed at study entry and at follow-up visits for a subset of subjects (see Shaw et al. 5 for details on biomarker acquisition).”
- Human apoE isoforms differentially regulate brain amyloid-β peptide clearance (2011, neutral): “Several groups have now validated molecular and neuroimaging biomarkers of the neuropathological hallmarks of AD (15-19).”
- 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, background): “For example, the tTau/ Ab(1–42) ratio was shown to predict MCI conversion to probable AD over 1 year [43] and the baseline tTau/ Ab(1–42) ratio indicated progression from MCI to dementia over 4–6 years, with a PPA of 95% and a NPA of 83% [16].”
- Clinical Neurology and Epidemiology of the Major Neurodegenerative Diseases. (2018, methodology): “…(at residues 181 and 231) in combination with reduced levels of soluble Ab1-42 amyloid distinguish AD patients from controls based on imaging tests (Shaw et al. 2009) and correlate with the presence of AD pathology at autopsy (Tapiola et al. 2009; reviewed in Blennow and Hampel 2003; Blennow et…”
- Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Early in the development of Alzheimer’s disease, the concentration of Aβ42 in the cerebrospinal fluid (CSF) starts to fall (Shaw et al. 2009), while the concentration of Aβ42 in the brain is rising (Steinerman et al. 2008), suggesting a diminution in Aβ transport from the brain, a result strongly…”
- Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia. (2011, background): “These include pathogenic mutations for other conditions (e.g. Presenilin, APP), extensive amyloid related radioligand binding (e.g. PIB) (Rabinovici et al., 2007), or the presence of sensitive and specific CSF markers (Dubois et al., 2000; Rowe et al., 2007; Shaw et al., 2009).”
- Biomarkers for Alzheimer's disease: academic, industry and regulatory perspectives (2010, neutral): “A high diagnostic performance of these CSF biomarkers has been verified in three large multicentre studies, including the Alzheimer's disease Neuroimaging Initiative (ADNI) stud”