scholarly journals Benzothiazolium Derivative-Capped Silica Nanocomposites for β-Amyloid Imaging In Vivo

Author(s):  
Lijun Ma ◽  
Shu Yang ◽  
Yufan Ma ◽  
Yuzhi Chen ◽  
Zhenguo Wang ◽  
...  
2004 ◽  
pp. 191-199 ◽  
Author(s):  
N. P. L. G. Verhoeff ◽  
A. A. Wilson ◽  
H. F. Kung ◽  
D. Hussey ◽  
L. Trop ◽  
...  

2004 ◽  
Vol 25 ◽  
pp. S58-S59 ◽  
Author(s):  
Nicolaas P. Verhoeff ◽  
Alan A. Wilson ◽  
Jose Nobrega ◽  
David Westaway ◽  
Peter St George-Hyslop ◽  
...  
Keyword(s):  

2009 ◽  
Vol 5 (4S_Part_1) ◽  
pp. P30-P30
Author(s):  
Milos D. Ikonomovic ◽  
Eric E. Abrahamson ◽  
Ronald L. Hamilton ◽  
Chester A. Mathis ◽  
Julie Price ◽  
...  

2011 ◽  
Vol 23 (S2) ◽  
pp. S41-S49 ◽  
Author(s):  
Victor L. Villemagne ◽  
Christopher C. Rowe

ABSTRACTMolecular neuroimaging techniques such as PET are proving valuable in the early and differential diagnosis of Alzheimer's disease (AD). With the advent of new therapeutic strategies aimed at reducing β-amyloid (Aβ) burden in the brain to potentially prevent or delay functional and irreversible cognitive loss, there is increased interest in developing agents that allow assessment of Aβ burden in vivo.Amyloid imaging with PET has proven useful in the discrimination of dementias, showing significantly higher Aβ burden in the gray matter of AD patients when compared with healthy controls or patients with frontotemporal dementia. ApoE ɛ4 carriers, independent of diagnosis or disease severity, present with higher Aβ burden than non-ɛ4 carriers. Amyloid imaging matches histopathological reports in aging and dementia, reflecting the true regional density of Aβ plaques in cortical areas. It also appears to be more sensitive than FDG-PET for the diagnosis of AD.In healthy older people there is an increasing prevalence of amyloid positive scans with age, rising from 20% in the seventh decade to 60% in the ninth decade. Of people with mild cognitive impairment (MCI), 40–60% present with detectable cortical Aβ deposition. In both groups, Aβ deposition is associated with a higher risk for cognitive decline and dementia due to AD. These observations suggest that Aβ deposition is not part of normal aging, supporting the hypothesis that it occurs well before the onset of symptoms and is likely to represent preclinical AD in asymptomatic persons and prodromal AD in MCI. Further longitudinal observations, coupled with different disease-specific tracers and biomarkers, are required to confirm this hypothesis and further elucidate the precise role of Aβ deposition in the course of AD.


2009 ◽  
Vol 5 (4S_Part_7) ◽  
pp. P202-P202
Author(s):  
Milos D. Ikonomovic ◽  
Eric E. Abrahamson ◽  
Ronald L. Hamilton ◽  
Chester A. Mathis ◽  
Julie Price ◽  
...  

Brain ◽  
2008 ◽  
Vol 131 (6) ◽  
pp. 1630-1645 ◽  
Author(s):  
Milos D. Ikonomovic ◽  
William E. Klunk ◽  
Eric E. Abrahamson ◽  
Chester A. Mathis ◽  
Julie C. Price ◽  
...  

2006 ◽  
Vol 59 (10) ◽  
pp. 940-947 ◽  
Author(s):  
Lisa Nichols ◽  
Victor W. Pike ◽  
Lisheng Cai ◽  
Robert B. Innis

2011 ◽  
Vol 21 (14) ◽  
pp. 4193-4196 ◽  
Author(s):  
Mengchao Cui ◽  
Masahiro Ono ◽  
Hiroyuki Kimura ◽  
Boli Liu ◽  
Hideo Saji

Author(s):  
Alex E. Roher ◽  
Kenneth C. Palmer ◽  
John Capodilupo ◽  
Arun R. Wakade ◽  
Melvyn J. Ball

ABSTRACT:Purification of amyloid plaque core proteins (APCP) from Alzheimer's disease brains to complete homogeneity and in high yield permitted its chemical fractionation and characterization of its components. APCP is mainly made of β-amyloid (βA) and an assortment of glycoproteins (accounting for 20%) rich in carbohydrates compatible with N-and O-linked saccharides. When added to tissue culture of sympathetic and sensory neurons APCP and βA inhibited neuritic sprouting, a reversible phenomenon at low doses. Higher concentrations of both substances kill the neurons in culture. APCP is significantly more toxic than βA, suggesting the minor components may play an important role in increasing the toxicity of βA. If the observed toxic effects of APCP in situ are occurring in vivo during the course of AD, then the accumulation of these extracellular proteins could be largely responsible for some of the neuronal death observed in this neuropathology.


2015 ◽  
Vol 44 (7) ◽  
pp. 1807-1819 ◽  
Author(s):  
Matteo Staderini ◽  
María Antonia Martín ◽  
Maria Laura Bolognesi ◽  
J. Carlos Menéndez

Near infrared (NIR) imaging is a promising and non-invasive method to visualize amyloid plaquesin vivo.


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