Sentences with phrase «transgenic ad model»

Importantly, this is one of the first reports applying Aβ immunoprecipitation followed by MALDI - MS analysis in CSF from a transgenic AD model, providing a robust, novel platform for the assessment of Aβ expression profiles in biological fluids of transgenic models.

High - Throughput Phenotyping of Transgenic AD Models D. BRUNNER, T. HANANIA, M. MAZZELLA, H. HAIN, E. SABATH, V. ALEXANDROV, J. BERGER, P. KABITZKE, K. COX, M. WINDISCH... Abstract / Posters

Not exact matches

First author Antonio Di Meco and colleagues used a triple transgenic (3xTg) mouse model that displays an AD - like phenotype, including cognitive decline, and Aβ and tau neuropathology characteristic of the disease in humans.

These use a high - throughput screening approach combined with MALDI - IMS to assess the specificity of those drugs on a transgenic mouse model of AD.

We measured Vc in axons of Schaffer collaterals in CA1 area of hippocampus in two transgenic mouse models of AD that over-express β - amyloid, line 41 (6mo) and APP / PS1 (24mo).

Second, we propose to test the effect of chronic or acute treatment with ApoA - I - Milano in a transgenic mouse model of AD.

In her translational research program, Dr. Duff has created several transgenic mouse models for Alzheimer's disease (AD) to explore disease mechanisms and test therapeutic approaches.

In a transgenic mouse model of AD, aducanumab is shown to enter the brain, bind parenchymal Aβ, and reduce soluble and insoluble Aβ in a dose - dependent manner.

For such study, we have used the McGill - R - Thy1 - APP transgenic rat, which is unique compared to other rodent models in that the AD - like phenotype has been achieved with a single genomic insertion of a mutated human APP transgene; minimizing off - target genetic corruption and therefore being closer to the human disease [32].

Given the lack of definitive AD biomarkers in humans, transgenic animal models of the amyloid pathology continue to be valuable tools to examine molecular changes preceding the deposition of amyloid plaques and associated pathology (i.e. late inflammation, neuritic dystrophy, etc.).