scholarly journals Cerebellar Amyloid-β Plaques: Disturbed Cortical Circuitry in AβPP/PS1 Transgenic Mice as a Model of Familial Alzheimer's Disease

2012 ◽  
Vol 31 (2) ◽  
pp. 285-300 ◽  
Author(s):  
Selene Lomoio ◽  
Irene López-González ◽  
Ester Aso ◽  
Margarita Carmona ◽  
Benjamín Torrejón-Escribano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Familial Alzheimer’S Disease ◽  
Cortical Circuitry ◽  
Familial Alzheimer's Disease

scholarly journals Heavy Tau Burden with Subtle Amyloid β Accumulation in the Cerebral Cortex and Cerebellum in a Case of Familial Alzheimer’s Disease with APP Osaka Mutation

2020 ◽  
Vol 21 (12) ◽  
pp. 4443
Author(s):  
Hiroyuki Shimada ◽  
Shinobu Minatani ◽  
Jun Takeuchi ◽  
Akitoshi Takeda ◽  
Joji Kawabe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Neuronal Degeneration ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Familial Alzheimer’S Disease ◽  
Pet Tracer ◽  
Familial Alzheimer's Disease ◽  
Parietal Cortices

We previously identified a novel mutation in amyloid precursor protein from a Japanese pedigree of familial Alzheimer’s disease, FAD (Osaka). Our previous positron emission tomography (PET) study revealed that amyloid β (Aβ) accumulation was negligible in two sister cases of this pedigree, indicating a possibility that this mutation induces dementia without forming senile plaques. To further explore the relationship between Aβ, tau and neurodegeneration, we performed tau and Aβ PET imaging in the proband of FAD (Osaka) and in patients with sporadic Alzheimer’s disease (SAD) and healthy controls (HCs). The FAD (Osaka) patient showed higher uptake of tau PET tracer in the frontal, lateral temporal, and parietal cortices, posterior cingulate gyrus and precuneus than the HCs (>2.5 SD) and in the lateral temporal and parietal cortices than the SAD patients (>2 SD). Most noticeably, heavy tau tracer accumulation in the cerebellum was found only in the FAD (Osaka) patient. Scatter plot analysis of the two tracers revealed that FAD (Osaka) exhibits a distinguishing pattern with a heavy tau burden and subtle Aβ accumulation in the cerebral cortex and cerebellum. These observations support our hypothesis that Aβ can induce tau accumulation and neuronal degeneration without forming senile plaques.

The genetic defect in familial Alzheimer's disease is not tightly linked to the amyloid β-protein gene

Nature ◽  
1987 ◽  
Vol 329 (6135) ◽  
pp. 156-157 ◽  
Author(s):  
Rudolph E. Tanzi ◽  
Peter H. St George-Hyslop ◽  
Jonathan L. Haines ◽  
Ronald J. Polinsky ◽  
Linda Nee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Gene ◽  
Genetic Defect ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Β Protein ◽  
Familial Alzheimer's Disease

scholarly journals Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer's Disease Mutations

2010 ◽  
Vol 176 (1) ◽  
pp. 353-368 ◽  
Author(s):  
Miguel A. Gama Sosa ◽  
Rita De Gasperi ◽  
Anne B. Rocher ◽  
Athena Ching-Jung Wang ◽  
William G.M. Janssen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Vascular Pathology ◽  
Presenilin 1 ◽  
Familial Alzheimer’S Disease ◽  
Age Related ◽  
Disease Mutations ◽  
Familial Alzheimer's Disease

scholarly journals Effects of Familial Alzheimer’s Disease Mutations on the Folding Nucleation of the Amyloid β-Protein

2008 ◽  
Vol 381 (1) ◽  
pp. 221-228 ◽  
Author(s):  
Mary Griffin Krone ◽  
Andrij Baumketner ◽  
Summer L. Bernstein ◽  
Thomas Wyttenbach ◽  
Noel D. Lazo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Disease Mutations ◽  
Β Protein ◽  
Familial Alzheimer's Disease
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