scholarly journals Cerebral Cortex and Hippocampal Protection Mediated by Callistemon viminalis in Aluminium Chloride Induced Alzheimer’s Disease

2020 ◽  
Vol 54 (2) ◽  
pp. 422-431
Author(s):  
Mandeep Singh ◽  
Yash Prashar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Aluminium Chloride ◽  
Callistemon Viminalis

Alzheimer's disease-type neurofibrillary degeneration in verrucose dysplasias of the cerebral cortex

1995 ◽  
Vol 90 (4) ◽  
pp. 356-365 ◽  
Author(s):  
M. A. Mor�n ◽  
A. Probst ◽  
C. Navarro ◽  
P. G�mez-Ramos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Disease Type ◽  
Neurofibrillary Degeneration

Intralaminar Distribution of Neurotransmitter-Related Enzymes in Cerebral Cortex of Alzheimer’s Disease

Gerontology ◽  
1987 ◽  
Vol 33 (3-4) ◽  
pp. 197-202 ◽  
Author(s):  
Sandro Sorbi ◽  
Silvia Piacentini ◽  
Luigi Amaducci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex

Columnar arragement of ?-amyloid protein deposits in the cerebral cortex of patients with Alzheimer's disease

1993 ◽  
Vol 85 (4) ◽  
pp. 400-403 ◽  
Author(s):  
H. Akiyama ◽  
T. Yamada ◽  
P. L. McGeer ◽  
T. Kawamata ◽  
I. Tooyama ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Amyloid Protein ◽  
Protein Deposits

Effect of artesunate in an animal model of Aluminium chloride induced alzheimer's disease

2021 ◽  
Vol 14 (2) ◽  
pp. 633-639
Author(s):  
Praveen S E Kumar ◽  
K L Bairy ◽  
Veena Nayak ◽  
Mohandas Rao ◽  
Shiva Kumar Reddy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Aluminium Chloride

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.

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