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Alzheimer's Disease / Frontotemporal Dementia

Alzheimer’s disease (AD) is the most common cause of dementia and afflicts about 36 million people worldwide. The pathogenesis is still unclear, although may support the Amyloid cascade theory, which is based on abnormal APP processing and clearance, leading to formation of toxic amyloid oligomers, fibrils and extracellular amyloid plaques. Amyloid seems to trigger the tau protein dependent neurofibrillary pathology, which is another pathological hallmark of AD. The whole process is long lasting and may start decades before first disease symptoms occur.

In spite of enormous research efforts so far no efficient treatment is available. For successful drug development, validated predictive animal models are needed. Genetically modified rodent models, expressing human (wild type or mutated) APP or human Tau (wildtype or mutated) replicate aspects of the pathogenetic cascade and provide useful tools for assessing the therapeutic potential of new treatment strategies. The value of these models is critically depending on the experience and skills of the investigators, strictly following principles of good scientific practice. Fully blinded randomized studies, based on power calculation are a standard for PsychoGenics.

PsychoGenics currently offers research with 3 different APP transgenic rodent models which are different in the time course of development of onset of Abeta-pathology, progression pattern, neuro-inflammation and cognitive deficits. In addition an advanced model of tau-pathology is available. In these mice a tetracycline responsive element allows control of tau expression (TET-off).

Amyloidosis Models

Tauopathy Model

  • PsychoGenics
  • 765 Old Saw Mill River Road, Tarrytown, NY 10591
  • tel: (914) 406-8019
  • fax: (914) 593-0645