Amyloid‐induced neurofibrillary tangle formation in Alzheimer's disease: insight from transgenic mouse and tissue‐culture models

2004 ◽  
Vol 22 (7) ◽  
pp. 453-465 ◽  
Author(s):  
Jürgen Götz ◽  
Andreas Schild ◽  
Fred Hoerndli ◽  
Luis Pennanen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tissue Culture ◽  
Transgenic Mouse ◽  
Neurofibrillary Tangle ◽  
Culture Models

Decreased Glucose Metabolism and Glutamine Synthesis in the Retina of a Transgenic Mouse Model of Alzheimer’s Disease

2021 ◽  
Author(s):  
Anna Luna Mølgaard Tams ◽  
Berta Sanz-Morello ◽  
Emil Winther Westi ◽  
Zaynab Ahmad Mouhammad ◽  
Jens Velde Andersen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Metabolism ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Glutamine Synthesis

scholarly journals Disruption of a RAC1-centred network is associated with Alzheimer’s disease pathology and causes age-dependent neurodegeneration

2020 ◽  
Vol 29 (5) ◽  
pp. 817-833 ◽  
Author(s):  
Masataka Kikuchi ◽  
Michiko Sekiya ◽  
Norikazu Hara ◽  
Akinori Miyashita ◽  
Ryozo Kuwano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Model ◽  
Neurofibrillary Tangle ◽  
Neuronal Cell ◽  
Brain Regions ◽  
Protein Domain ◽  
Expression Data ◽  
Integrated Network ◽  
Age Dependent

Abstract The molecular biological mechanisms of Alzheimer’s disease (AD) involve disease-associated crosstalk through many genes and include a loss of normal as well as a gain of abnormal interactions among genes. A protein domain network (PDN) is a collection of physical bindings that occur between protein domains, and the states of the PDNs in patients with AD are likely to be perturbed compared to those in normal healthy individuals. To identify PDN changes that cause neurodegeneration, we analysed the PDNs that occur among genes co-expressed in each of three brain regions at each stage of AD. Our analysis revealed that the PDNs collapsed with the progression of AD stage and identified five hub genes, including Rac1, as key players in PDN collapse. Using publicly available as well as our own gene expression data, we confirmed that the mRNA expression level of the RAC1 gene was downregulated in the entorhinal cortex (EC) of AD brains. To test the causality of these changes in neurodegeneration, we utilized Drosophila as a genetic model and found that modest knockdown of Rac1 in neurons was sufficient to cause age-dependent behavioural deficits and neurodegeneration. Finally, we identified a microRNA, hsa-miR-101-3p, as a potential regulator of RAC1 in AD brains. As the Braak neurofibrillary tangle (NFT) stage progressed, the expression levels of hsa-miR-101-3p were increased specifically in the EC. Furthermore, overexpression of hsa-miR-101-3p in the human neuronal cell line SH-SY5Y caused RAC1 downregulation. These results highlight the utility of our integrated network approach for identifying causal changes leading to neurodegeneration in AD.

[P1-107]: APPKI-HaβWT: A NOVEL TRANSGENIC MOUSE TO MODEL SPORADIC ALZHEIMER's DISEASE

2017 ◽  
Vol 13 (7S_Part_5) ◽  
pp. P281-P281
Author(s):  
David Baglietto-Vargas ◽  
Lena Cai ◽  
Stefania Forner ◽  
Alessandra Martini ◽  
Celia Cunha ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Sporadic Alzheimer’S Disease
Sign in / Sign up

Export Citation Format

Share Document