scholarly journals Longitudinal, Quantitative Assessment of Amyloid, Neuroinflammation, and Anti-Amyloid Treatment in a Living Mouse Model of Alzheimer's Disease Enabled by Positron Emission Tomography

2007 ◽  
Vol 27 (41) ◽  
pp. 10957-10968 ◽  
Author(s):  
J. Maeda ◽  
B. Ji ◽  
T. Irie ◽  
T. Tomiyama ◽  
M. Maruyama ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Mouse Model ◽  
Quantitative Assessment ◽  
Emission Tomography ◽  
Model Of Alzheimer’S Disease ◽  
Positron Emission ◽  
Living Mouse

scholarly journals Studies of copper trafficking in a mouse model of Alzheimer's disease by positron emission tomography: comparison of64Cu acetate and64CuGTSM

Metallomics ◽  
2017 ◽  
Vol 9 (11) ◽  
pp. 1622-1633 ◽  
Author(s):  
Erica M. Andreozzi ◽  
Julia Baguña Torres ◽  
Kavitha Sunassee ◽  
Joel Dunn ◽  
Simon Walker-Samuel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Mouse Model ◽  
Amyloid Plaques ◽  
Emission Tomography ◽  
Copper Trafficking ◽  
Model Of Alzheimer’S Disease ◽  
Positron Emission ◽  
Selective Delivery

Positron emission tomography with64Cu demonstrates regionally selective delivery of copper to brain, which although modified in an Alzheimer's model, does not correlate with the location of amyloid plaques.

IC-P-024: A novel positron emission tomography contrast agent targeting cathepsin d shows preferential in vivo retention in an Alzheimer's disease mouse model

2015 ◽  
Vol 11 (7S_Part_1) ◽  
pp. P26-P27
Author(s):  
Jonatan A. Snir ◽  
Mojmir Suchy ◽  
Geron A. Bindseil ◽  
Blaine A. Chronik ◽  
Robert H.E. Hudson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Mouse Model ◽  
Contrast Agent ◽  
Cathepsin D ◽  
Emission Tomography ◽  
Positron Emission

O1-02-05: A novel positron emission tomography contrast agent targeting cathepsin d shows preferential in vivo retention in an Alzheimer's disease mouse model

2015 ◽  
Vol 11 (7S_Part_3) ◽  
pp. P128-P128
Author(s):  
Jonatan A. Snir ◽  
Mojmir Suchy ◽  
Geron A. Bindseil ◽  
Blaine A. Chronik ◽  
Robert H.E. Hudson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Mouse Model ◽  
Contrast Agent ◽  
Cathepsin D ◽  
Emission Tomography ◽  
Positron Emission

In vivoimaging of microglial activation by positron emission tomography with [11C]PBR28 in the 5XFAD model of Alzheimer's disease

Glia ◽  
2016 ◽  
pp. n/a-n/a ◽  
Author(s):  
Nazanin Mirzaei ◽  
Sac Pham Tang ◽  
Sharon Ashworth ◽  
Christopher Coello ◽  
Christophe Plisson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Microglial Activation ◽  
Emission Tomography ◽  
Model Of Alzheimer’S Disease ◽  
Positron Emission

scholarly journals The cortical origin and initial spread of medial temporal tauopathy in Alzheimer’s disease assessed with positron emission tomography

2021 ◽  
Vol 13 (577) ◽  
pp. eabc0655
Author(s):  
Justin S. Sanchez ◽  
J. Alex Becker ◽  
Heidi I. L. Jacobs ◽  
Bernard J. Hanseeuw ◽  
Shu Jiang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Amyloid Β ◽  
Emission Tomography ◽  
Model Of Alzheimer’S Disease ◽  
Positron Emission ◽  
Wide Range

Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer’s disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-β (Aβ) pathology to mediate neurodegeneration and cognitive decline. Initial TAU deposition occurs many years before Aβ in a specific area of the medial temporal lobe. Building on recent work that enabled focus of molecular PET measurements on specific TAU-vulnerable convolutional temporal lobe anatomy, we applied an automated anatomic sampling method to quantify TAU PET signal in 443 adult participants from several observational studies of aging and AD, spanning a wide range of ages, Aβ burdens, and degrees of clinical impairment. We detected initial cortical emergence of tauopathy near the rhinal sulcus in clinically normal people and, in a subset with longitudinal 2-year follow-up data (n = 104), tracked Aβ-associated spread of TAU from this site first to nearby neocortex of the temporal lobe and then to extratemporal regions. Greater rate of TAU spread was associated with baseline measures of both global Aβ burden and medial temporal lobe TAU. These findings are consistent with clinicopathological correlation studies of Alzheimer’s tauopathy and enable precise tracking of AD-related TAU progression for natural history studies and prevention therapeutic trials.

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