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Scientists seeking better mouse models for Alzheimer’s disease recently developed human mutant APP knock-ins (see related SfN story). The slowly developing pathology in these mice may better resemble ...
While amyloid-beta has been a central focus in drug development, increasing evidence points to tau pathology as a more accurate predictor of disease progression. This is where the work of Dr. Naoto ...
two groups have recently characterized knock-in mice with p53 ‘hot spot’ missense mutations (Lang et al., 2004; Olive et al., 2004). These mouse models support a gain-of-function phenotype ...
“There have been many TDP-43 models reported, but TDP-43-induced toxicity can be severe with a narrow gene dose-response,” wrote Ronald Klein of Louisiana State University in Shreveport. “This new ...
"It's not just another rodent model of Alzheimer's," Yu says ... and pathophysiology spontaneously developed in the GluN3A knockout mouse in an age-dependent manner," Yu says.
Using their knock-in mouse models, a likely cause of the progressive cognitive illness has been discovered. This could lead to new prevention and treatment opportunities for Alzheimer’s disease. The ...
The Genetically Engineered Rodent Models Core possesses specialized expertise and state ... targeted knockout, and targeted knock-in mouse lines. Knockout and knock-in mouse lines can be generated ...
The three key functions of the Core are listed below: These CF mouse models produce no functional Cftr mRNA or protein, and are particularly useful to stufy consequences of the electrophysiological ...
About a decade ago, U.S. scientists at the National Institutes of Health (NIH) developed a standard estrogen receptor (ER) gene knock-out mouse model to study the estrogen receptor’s role in ...
Since the founding of the program, KOMP2 scientists have adhered to uniform phenotyping protocols, data collection, and reporting standards, made all data available via on IMPC website, and deposited ...
"It's not just another rodent model of Alzheimer's," Yu says ... and pathophysiology spontaneously developed in the GluN3A knockout mouse in an age-dependent manner," Yu says.