Seed and spread Tauopathy model

Key characteristics

  • Unilateral stereotactic injection of hyperphosphorylated brainstem lysate or synthetic K18 preformed fibrils into the hippocampus
  • Progressive seeding and spreading of Tau pathology
  • Increased microgliosis and astrocytosis
  • Correlation between ipsi- and contralateral hippocampus
Alt

Successful seed and spreading of Tau pathology after unilateral injection of brain lysate of either old TauP301S mice with high levels of phosphorylated and aggregated Tau (Tau aggregates, n = 9) or from age-matched wild types (negative control, n =5) into the hippocampus. Stereotactic injection was performed at an age of 2 months. Pathological Tau particles (AT8) were quantified 9 weeks after injection, in both the ipsilateral (left) and contralateral (right) hippocampus as measured by IHC (mean ± SEM). Statistics: Welches’ unpaired t test.

Alt

Time course of Tau seeding and spreading after unilateral injection of brain lysate of either old TauP301L mice with high levels of phosphorylated and aggregated Tau (Tau aggregates, n = 8) or from age-matched wild types (negative control, n =6) into the hippocampus. Stereotactic injection was performed at an age of 3.2 months. Pathological Tau particles (AT8) were quantified 2, 3, 5, 9 and 13 weeks (control only at 13 weeks) after injection, in both the ipsilateral (left) and contralateral (right) hippocampus as measured by IHC (mean ± SEM). Statistics: Welches’ unpaired t test.

Interested to see more data?

We have a more extensive datapackage available. Contact us at cro[at]remynd.com to set up a meeting and discuss how we translate your mechanism of action into an effective study design.

Literature

Describing papers:

  • Original paper: Cfr TAU[P301S] or TAU[P301L]
  • Detrez et al., 2019: Regional vulnerability and spreading of hyperphosphorylated tau in seeded mouse brain. DOI: 10.1016/j.nbd.2019.03.010