• Our primary disease model is a transgenic mouse model carrying Swedish APP and Finnish PSEN1dE9 human gene mutations that cause rare familial forms of AD. Among numerous AD model mice this line is different in that amyloid plaque pathology starts early (~3 months of age) and is fully developed before memory impairment becomes evident (~12 months of age). This order of events corresponds to present understanding of the disease course.
  • Mouse neurological and neuropsychological testing.
    Through a broad behavioral test battery we can fully characterize the phenotype of AD mouse models and assess the effect of novel therapeutic approaches.
  • In vivo electrophysiology.
    By using multiple bi- or tripolar implanted microelectrodes into areas of interest, we can assess long-term changes in local electrical activity at any brain site, as well as to study the cross-talk between these brain sites. Recordings are combined with video monitoring, also during a memory task. We also combine EEG recordings with BOLD-fMRI in mice.
  • At the end of any study, the mouse brain is carefully examined for hallmarks of AD pathology (amyloid deposit, tau phosphorylation, neuroinflammation) and other processes of interest.
  • Gene transfer. By using viral vectors we can transduce production of any protein of interest locally in the brain to study the molecular interactions behind the memory problems or to reverse the pathological process in a treatment attempt.
  • Pre-clinical assessment of novel treatments including conventional drug candidates or dietary manipulations.