|Name||Other Names||Strain Name||Genetic Background||Gene||Mutation||Modification Info||Modification||Disease||Neuropathology||Behavior/Cognition||Other Phenotype||Availability||Primary Paper||Visualization|
Rat Models (1)
|Apphu/hu;Psen1M139T+/+||Long Evans||App, Psen1||PSEN1 M139T||Crispr/Cas9 was used to humanize the Aβ sequence within the rat App gene and to introduce the M139T mutation into the rat Psen1 gene.||App: Knock-In; Psen1: Knock-In||Alzheimer's Disease||No plaques or tangles were observed up to 2 years of age.||Unknown.||Elevated levels of CTFβ and Aβ compared with wild-type rats. Increased Aβ42/Aβ40 ratio relative to rats homozygous for humanized App, but without the Psen1 mutation.||Available through Lutgarde Serneels.||Serneels et al., 2020||Yes|
AD-related Research Models
- Neuronal Loss
- Synaptic Loss
- Changes in LTP/LTD
- Cognitive Impairment
When visualized, these phenotypes will distributed over a 18 month timeline demarcated at the following intervals: 3mo, 6mo, 9mo, 1yr, 15mo, 18mo+.
No plaques observed up to 2 years of age.
No tangles observed up to 2 years of age.
Neuronal Loss at
Synaptic Loss at
Changes in LTP/LTD at
Cognitive Impairment at
|App, Psen1||PSEN1 M139T||App: Knock-In; Psen1: Knock-In||Alzheimer's Disease||
No plaques or tangles were observed up to 2 years of age.