Aβ38 in the Brains of Patients with Sporadic and Familial Alzheimer's Disease and Transgenic Mouse Models

2014 ◽  
Vol 39 (4) ◽  
pp. 871-881 ◽  
Author(s):  
Jochim Reinert ◽  
Henrik Martens ◽  
Melanie Huettenrauch ◽  
Tekla Kolbow ◽  
Lars Lannfelt ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Transgenic Mouse Models ◽  
Familial Alzheimer’S Disease ◽  
Familial Alzheimer's Disease

scholarly journals Brain Biomarkers in Familial Alzheimer’s Disease Mouse Models

2017 ◽  
Vol 60 (3) ◽  
pp. 949-958 ◽  
Author(s):  
Yafit Kuttner-Hirshler ◽  
Palamadai N. Venkatasubramanian ◽  
Joan Apolinario ◽  
Jacqueline Bonds ◽  
Alice M. Wyrwicz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Familial Alzheimer’S Disease ◽  
Familial Alzheimer's Disease

scholarly journals Secondary Metabolites from Plants Possessing Inhibitory Properties against Beta-Amyloid Aggregation as Revealed by Thioflavin-T Assay and Correlations with Investigations on Transgenic Mouse Models of Alzheimer’s Disease

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 870 ◽  
Author(s):  
Raluca Stefanescu ◽  
Gabriela Dumitriṭa Stanciu ◽  
Andrei Luca ◽  
Luminita Paduraru ◽  
Bogdan-Ionel Tamba
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Secondary Metabolites ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Beta Amyloid ◽  
Thioflavin T ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Study Results

Alzheimer’s disease is a neurodegenerative disorder for which there is a continuous search of drugs able to reduce or stop the cognitive decline. Beta-amyloid peptides are composed of 40 and 42 amino acids and are considered a major cause of neuronal toxicity. They are prone to aggregation, yielding oligomers and fibrils through the inter-molecular binding between the amino acid sequences (17–42) of multiple amyloid-beta molecules. Additionally, amyloid deposition causes cerebral amyloid angiopathy. The present study aims to identify, in the existing literature, natural plant derived products possessing inhibitory properties against aggregation. The studies searched proved the anti-aggregating effects by the thioflavin T assay and through behavioral, biochemical, and histological analysis carried out upon administration of natural chemical compounds to transgenic mouse models of Alzheimer’s disease. According to our present study results, fifteen secondary metabolites from plants were identified which presented both evidence coming from the thioflavin T assay and transgenic mouse models developing Alzheimer’s disease and six additional metabolites were mentioned due to their inhibitory effects against fibrillogenesis. Among them, epigallocatechin-3-gallate, luteolin, myricetin, and silibinin were proven to lower the aggregation to less than 40%.

Genotype-related changes of ganglioside composition in brain regions of transgenic mouse models of Alzheimer's disease

2007 ◽  
Vol 28 (12) ◽  
pp. 1863-1872 ◽  
Author(s):  
Laurence Barrier ◽  
Sabrina Ingrand ◽  
Milena Damjanac ◽  
Agnès Rioux Bilan ◽  
Jacques Hugon ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Brain Regions ◽  
Transgenic Mouse Models ◽  
Ganglioside Composition
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