Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans

By Anne M. Fagan, Mark A. Mintun, R. Mach, Sang-Yoon Lee, C. Dence, Aarti R. Shah, Gina N. LaRossa, Michael L. Spinner, William E. Klunk, Chester A. Mathis and 3 more. Annals of Neurology, 2006

946 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/e31fda275d4ce96980c0fda16596259a20335daa

How researchers see this paper

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In Cellular and Molecular Neuroscience

1. Yaakov Stern
2. David S. Knopman
3. Reisa A. Sperling
4. Guy M. McKhann
5. Clifford R. Jack Jr.
6. D. Holtzman
7. C. Phelps

In Physiology

1. D. Holtzman
2. Clifford R. Jack Jr.
3. Reisa A. Sperling
4. Richard P. Mayeux
5. Yaakov Stern
6. Ronald C. Petersen
7. Brad Boeve
8. David S. Knopman

In Psychiatry and Mental health

1. Clifford R. Jack Jr.
2. D. Holtzman
3. Ronald C. Petersen
4. Richard P. Mayeux
5. Reisa A. Sperling
6. David S. Knopman
7. Yaakov Stern
8. Brad Boeve

Citations in the corpus

• Fibrillar amyloid-β burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease (2009, result): “In a previous study, increased cerebral PiB binding was found to be associated with lower CSF A 42 concentrations (33), supporting the use of either measurement as an indicator of fibrillar A burden.”
• Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease (2016, neutral): “CSF (20 to 30 ml) was collected after overnight fasting as described previously (48, 49).”