PET of brain amyloid and tau in mild cognitive impairment.

By G. Small, V. Kepe, L. Ercoli, P. Siddarth, Susan Y. Bookheimer, K. Miller, H. Lavretsky, A. Burggren, G. Cole, H. Vinters and 5 more. New England Journal of Medicine, 2006

679 citations recorded by the source corpus.

Subfields: Physiology, Psychiatry and Mental health, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/49a4b3d394c56f29ef0dc53726204c199a1df181

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Citations in the corpus

18F‐flutemetamol amyloid imaging in Alzheimer disease and mild cognitive impairment: A phase 2 trial (2010, background): “The primary analysis was based on the 27 AD subjects who received an 18F-flutemetamol scan and the 15 elderly HVs. Images were presented with the lower intensity limit defined by the minimum in the 3-dimensional (3D) image (usually zero) and the maximum scaled to the 3D dataset voxel peak value and ”
Multi-modal techniques for diagnosis and prognosis of Alzheimer’s disease (2009, background): “One of these, [ 18 F]FDDNP, may be retained by NFT”
The Episodic Memory System: Neurocircuitry and Disorders (2009, neutral): “Recently, revolutionary new imaging technology using molecular ligands that bind to pathologic protein forms that accumulate in the AD brain is illuminating the localization and severity of pathology in various brain regions in living patients (Klunk et al, 2004; Small et al, 2006).”
The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals (2008, background): “…known to occur in the disease from post-mortem studies (Brun and Gustafson 1976; Arnold et al. 1991; Braak and Braak 1991) and from recent in vivo PET investigations using tracers that bind to pathologic proteins (Klunk et al. 2004; Buckner et al. 2005; Mintun et al. 2006; Small et al. 2006).”
Molecular mechanisms and physiological functions of mitophagy (2021, neutral): “Accumulation of insoluble b -amyloid plaques and formation of neurofibrillary tangles (aggregates of hyperphosphory-lated tau proteins) in brain are the major pathological hallmarks of AD (Small et al , 2006; Querfurth & LaFerla, 2010).”
Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease (2008, background): “Positron emission tomography (PET) imaging of amyloid deposits (Klunk et al., 2004; Verhoeff et al., 2004; Small et al., 2006) employs blood–brain barrier penetrant amyloid-binding compounds such as the thioflavin-T derivative Pittsburgh Compound-B (PiB) (Klunk et al., 2001, 2004; Mathis et al.,…”
11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment. (2008, background): “The most significant advance in dementia imaging in recent years has been the development of in vivo amyloid plaque labeling compounds (Klunk et al., 2004; Small et al., 2006; Verhoeff et al., 2004).”
Automated MRI measures identify individuals with mild cognitive impairment and Alzheimer's disease (2009, neutral): “radioactive amyloid and tau protein tracer (Small et al., 2006) and two prior MRI studies where a smaller number of subjects”