[11C]PIB in a nondemented population
By Mark A. Mintun, Gina N. LaRossa, Yvette I. Sheline, C. Dence, S. Lee, R. Mach, William E. Klunk, Chester A. Mathis, Steven DeKosky, J. Morris. Neurology, 2006
687 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/386d960db7752b1bc910cda9440b23d0d6fa5e9a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- D. Holtzman
- Daniel L. Schacter
- Jessica R. Andrews-Hanna
- Randy L. Buckner
- Robert A. Koeppe
- Reisa A. Sperling
- Michael W. Weiner
- Clifford R. Jack Jr.
In Physiology
- D. Holtzman
- Clifford R. Jack Jr.
- Reisa A. Sperling
- Randy L. Buckner
- Ronald C. Petersen
- Brad Boeve
- William E. Klunk
- Jessica R. Andrews-Hanna
In Psychiatry and Mental health
- D. Holtzman
- Clifford R. Jack Jr.
- Reisa A. Sperling
- Ronald C. Petersen
- Randy L. Buckner
- Brad Boeve
- Jessica R. Andrews-Hanna
- Keith A. Johnson
Citations in the corpus
- APOE Predicts Aβ but not Tau Alzheimer’s Pathology in Cognitively Normal Aging (2010, methodology): “Data from many of the 241 participants have appeared in previous reports from our ADRC.(20,61,67)”
- In Vivo Imaging of Amyloid Deposition in Alzheimer’s Disease using the Novel Radioligand [18F]AV-45 (Florbetapir F 18) (2010, background): “This pattern is similar to that previously reported for 11CPIB (21,22) and 18F-BAY94-9172 (9).”
- The Brain's Default Network (2008, background): “The map of rest-state glycolysis correlates remarkably well with the distribution of amyloid plaques (Mintun et al. 2006a).”
- 11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment. (2008, background): “However, approximately 30% of CN subjects demonstrate amyloid retention levels in cortex which are in the typical range for AD (Mintun et al., 2006).”
- Cortical Hubs Revealed by Intrinsic Functional Connectivity: Mapping, Assessment of Stability, and Relation to Alzheimer’s Disease (2009, methodology): “Coupled with the recent observation that glycolysis is preferentially high in regions associated with the default network (Mintun et al., 2006b), it is also possible that connectional hubs may mediate their influence on A deposition through glycolytic metabolism, although a mechanism linking…”
- OASIS-3: Longitudinal Neuroimaging, Clinical, and Cognitive Dataset for Normal Aging and Alzheimer Disease (2019, neutral): “Binding potential (BPND) is calculated using Logan graphical analysis 42,43,49–51 , for full dynamic PET imaging data are available, i.e. PET acquisition was started in synchronization with tracer administration and PET images were reconstructed into multiple time frames.”
- Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease (2016, neutral): “Topographic studies of AD-related pathology in vivo, until recently, have been limited to fibrillar Aβ (4, 5) owing to a lack of positron emission tomography (PET) imaging agents for tau pathology.”
- Multi-modal techniques for diagnosis and prognosis of Alzheimer’s disease (2009, result): “Notably, an appreciable number of cognitively normal individuals over the age of 60 show a PIB signal pattern indistinguishable from that of individuals with Alzheimer's disease, suggesting that measurement of PIB using PET can detect a preclinical stage of the diseas”