IC-P-126: Divergent pattern of changes in astrocytosis and fibrillar amyloid plaques as measured by PET in autosomal-dominant and sporadic Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_2) ◽  
pp. P86-P86
Author(s):  
Elena Rodriguez-Vieitez ◽  
Stephen F. Carter ◽  
Laure Saint-Aubert ◽  
Ove Almkvist ◽  
Karim Farid ◽  
...  
2015 ◽  
Vol 11 (7S_Part_3) ◽  
pp. P127-P127
Author(s):  
Elena Rodriguez-Vieitez ◽  
Stephen F. Carter ◽  
Laure Saint-Aubert ◽  
Ove Almkvist ◽  
Karim Farid ◽  
...  

2015 ◽  
Vol 11 (7S_Part_19) ◽  
pp. P878-P878
Author(s):  
Ruiqing Ni ◽  
Per-Göran Gillberg ◽  
Matti Viitanen ◽  
Liisa Myllykangas ◽  
Nenad Bogdanovic ◽  
...  

2021 ◽  
Author(s):  
Elizabeth Levitis ◽  
Jacob W Vogel ◽  
Thomas Funck ◽  
Vladimir Halchinski ◽  
Serge Gauthier ◽  
...  

Amyloid-beta (Aβ) deposition is one of the hallmark pathologies in both sporadic Alzheimer's disease (sAD) and autosomal dominant Alzheimer's disease (ADAD), the latter of which is caused by mutations in genes involved in Aβ processing. Despite Aβ deposition being a centerpiece to both sAD and ADAD, some differences between these AD subtypes have been observed with respect to the spatial pattern of Aβ. Previous work has shown that the spatial pattern of Aβ in individuals spanning the sAD spectrum can be reproduced with high accuracy using an epidemic spreading model (ESM), which simulates the diffusion of Aβ across neuronal connections and is constrained by individual rates of Aβ production and clearance. However, it has not been investigated whether Aβ deposition in the rarer ADAD can be modeled in the same way, and if so, how congruent the spreading patterns of Aβ across sAD and ADAD are. We leverage the ESM as a data-driven approach to probe individual-level variation in the spreading patterns of Aβ across three different large-scale imaging datasets (2 SAD, 1 ADAD). We applied the ESM separately to the Alzheimer's Disease Neuroimaging initiative (N=737), the Open Access Series of Imaging Studies (N=510), and the Dominantly Inherited Alzheimer's Network (N=249), the latter two of which were processed using an identical pipeline. We assessed inter- and intra-individual model performance in each dataset separately, and further identified the most likely epicenter of Aβ spread for each individual. Using epicenters defined in previous work in sAD, the ESM provided moderate prediction of the regional pattern of Aβ deposition across all three datasets. We further find that, while the most likely epicenter for most Aβ-positive subjects overlaps with the default mode network, 13% of ADAD individuals were best characterized by a striatal origin of Aβ spread. These subjects were also distinguished by being younger than ADAD subjects with a DMN Aβ origin, despite having a similar estimated age of symptom onset. Together, our results suggest that most ADAD patients express Aβ spreading patters similar to those of sAD, but that there may be a subset of ADAD patients with a separate, striatal phenotype.


2020 ◽  
Vol 16 (S6) ◽  
Author(s):  
Sanjay Pawar ◽  
Lucy Montoya ◽  
Lillibeth Barrera ◽  
Livier Mora ◽  
Kristyan Cortez‐Sanchez ◽  
...  

2018 ◽  
Vol 14 (12) ◽  
pp. 1632-1639 ◽  
Author(s):  
Gaël Nicolas ◽  
Rocío Acuña-Hidalgo ◽  
Michael J. Keogh ◽  
Olivier Quenez ◽  
Marloes Steehouwer ◽  
...  

2006 ◽  
Vol 14 (7S_Part_2) ◽  
pp. P134-P134
Author(s):  
Julie Gonneaud ◽  
Christophe Bedetti ◽  
Alexa Pichet Binette ◽  
Tammie L.S. Benzinger ◽  
John C. Morris ◽  
...  

2013 ◽  
Vol 9 ◽  
pp. P252-P253
Author(s):  
Jewell Thomas ◽  
Matthew Brier ◽  
Randall Bateman ◽  
Abraham Snyder ◽  
Tammie Benzinger ◽  
...  

2017 ◽  
Vol 133 (6) ◽  
pp. 933-954 ◽  
Author(s):  
Eleanor Drummond ◽  
Shruti Nayak ◽  
Arline Faustin ◽  
Geoffrey Pires ◽  
Richard A. Hickman ◽  
...  

2006 ◽  
Vol 14 (7S_Part_8) ◽  
pp. P469-P470
Author(s):  
Julie Gonneaud ◽  
Christophe Bedetti ◽  
Alexa Pichet Binette ◽  
Tammie L.S. Benzinger ◽  
John C. Morris ◽  
...  

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