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Alzheimers Disease Transgenic Mouse Models

Alzheimer’s disease (AD) is one of the most devastating neurodegenerative diseases of the 21st century and it accounts for 60-80% of all dementia cases. The most significant known risk factor for AD is advancing age, with most individuals being at least 65 years old when diagnosed. AD is a progressive condition, characterized by the gradual worsening of dementia symptoms over time. Two pathological hallmarks, plaques and tangles, are commonly suspected as being responsible for neurodegenerative processes in AD.

  • Plaques: Deposits of a protein fragment called amyloid-β that accumulate in spaces between nerve cells.
  • Tangles: Twisted fibers of tau protein that form inside nerve cells.

Experts in the field have debated for decades whether amyloid-β or tau is the better target to cure AD. We cannot answer this question but we can offer an extensive CRO service with transgenic mouse models for both aspects of the disease.

Scantox currently offers several human APP and Tau transgenic mouse lines featuring different properties regarding Aβ and tau expression patterns, neuroinflammation, cognitive deficits, age at onset and progression of pathology. These animals focus on different pathological readouts and constitute suitable models to study the influence of drugs on APP- or tau- related brain pathology and behavior.

Scantox offers custom tailored study design for these models, and we are flexible to accommodate to your special interests. We are also happy to advice you and propose study designs. Scantox maintains its own colonies directly in our research facility. Non-transgenic littermates are available as control animals needed for proper study design.

We would be happy to test your compounds in these mouse models! Readouts depend on model but the most common are:

  • Aβ-38,-40 and -42 levels
  • Aggregated Amyloid levels by A4 Assay
  • Plaque load
  • β-sheet load
  • pE(3)-Aβ load
  • Total tau and phosphorylated tau at different residues
  • Neurofilament Light Chain levels
  • Neuronal loss
  • Synaptic alterations
  • Oxidative stress
  • Neuroinflammation
  • Cerebral vascular angiopathy (CAA)
  • Blood brain barrier homeostasis
  • Learning and memory deficits (MWM)
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We are happy to receive your inquiry.