Two-year follow-up of amyloid deposition in patients with Alzheimer's disease.
By H. Engler, A. Forsberg, O. Almkvist, G. Blomquist, E. Larsson, I. Savitcheva, A. Wall, Anna Ringheim, B. Långström, A. Nordberg. Brain : a journal of neurology, 2006
650 citations recorded by the source corpus.
Subfields: Neurology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/647a98b263df3ce7792380938477d9a916a14c13
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Neurology
- Ronald C. Petersen
- Nick C Fox
- Clement Hamani
- William E. Klunk
- Reisa A. Sperling
- Clifford R. Jack Jr.
- Ronald L. Hamilton
- Steven DeKosky
In Physiology
- Clifford R. Jack Jr.
- Reisa A. Sperling
- Ronald C. Petersen
- Brad Boeve
- Nick C Fox
- William E. Klunk
- Chester A. Mathis
- Keith A. Johnson
In Psychiatry and Mental health
- Clifford R. Jack Jr.
- Ronald C. Petersen
- Reisa A. Sperling
- Brad Boeve
- Nick C Fox
- Keith A. Johnson
- Chester A. Mathis
- William E. Klunk
Citations in the corpus
- BRAIN FUEL METABOLISM, AGING AND ALZHEIMER’S DISEASE (2010, background): “A combination of PET imaging methods that simultaneously measures brain glucose metabolism and β-amyloid deposition could improve the diagnosis and/or prognosis of AD, especially if applied longitudinally [43,193].”
- Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade (2010, neutral): “62 ,81 1).”
- Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer's disease: implications for sequence of pathological events in Alzheimer's disease (2009, neutral): “Published estimates indicate an expected test/retest reliability of (cid:2) 7% for PIB imaging (Lopresti et al ., 2005; Engler et al ., 2006).”
- A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease (2010, background): “The sensitivity of amyloid imaging for diagnosis, prognosis, and longitudinal AD progression are improved considerably, however, when amyloid imaging is combined with measures of neuronal dysfunction, such as cerebral glucose metabolism or brain volume.(10,14,15) Although details of the mechanism re”
- Brain imaging in Alzheimer disease. (2012, background): “plateaued (Engler et al. 2006; Jack et al. 2009), but FDG continues to decline along with cognitive function (Engler et al.”
- Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease (2008, background): “Although the PiBPET study and autopsy were separated by 10 months, Engler et al. (2006) have shown that PiB-PET DVR values do not change appreciably over 2 years in patients with Alzheimer’s disease.”
- 11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment. (2008, background): “To date, most diagnostic imaging comparisons between amyloid labeling ligands and other imaging modalities have been between PiB and FDG-PET (Edison et al., 2007; Engler et al., 2006; Forsberg et al., 2007).”