Research Models

Selected Results

1 Models

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)
<p>-</p>, <p>App<sup>hu/hu</sup>;Psen1M139T<sup>+/+</sup></p> 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

1 Visualizations

AD-related Research Models

Phenotypes Examined

  • Plaques
  • Tangles
  • Neuronal Loss
  • Gliosis
  • 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+.

App knock-in (humanized Aβ) (Leuven); Psen1 knock-in (M139T)

Observed
Absent
  • Plaques at

    No plaques observed up to 2 years of age.

  • Tangles at

    No tangles observed up to 2 years of age.

No Data
  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
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.

Unknown.

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