Decreased beta-amyloid1-42 and increased tau levels in cerebrospinal fluid of patients with Alzheimer disease.
By T. Sunderland, G. Linker, N. Mirza, K. Putnam, David L. Friedman, L. Kimmel, Judy Bergeson, G. Manetti, M. Zimmermann, B. Tang and 2 more. Journal of the American Medical Association (JAMA), 2003
650 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/c92df2224c9f87e8a80a615f21156daa00962ae1
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In Cellular and Molecular Neuroscience
In Physiology
- D. Holtzman
- A. Goate
- John C. Morris
- Jungsu Kim
- Anne M. Fagan
- Richard Hargreaves
- Richard Frank
- D. Selkoe
In Psychiatry and Mental health
Citations in the corpus
- Human apoE isoforms differentially regulate brain amyloid-β peptide clearance (2011, positive): “In particular, low concentrations of Aβ42 in the cerebrospinal fluid (CSF) reflect the presence of cerebral Aβ deposition, likely as a result of Aβ42 being sequestered into amyloid plaques, changing the equilibrium between the brain and CSF pools of Aβ (20-22).”
- Clinical biomarkers in drug discovery and development (2003, background): “in blood, urine or cerebrospinal fluid have been proposed, the most obvious of which are β-amyloid and Tau proteins, as they seem to be intimately involved in the pathology of Alzheimer's diseas”
- Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults. (2007, neutral): “White 82 (91) 31 (94) 14 (87) African American 7 (8) 2 ( 6 ) 2 (13)”