The model expresses mutant human amyloid precursor protein (APPSW) and presenilin 1(PS1ΔE9) genes, according to the preclinical contract research organization (CRO).
Developed by Professor Robert Cohen, MD and a team at the National Institute of Mental Health (NIMH), part of NIH, the rat models develop Alzheimer’s disease symptoms that progress with age and become pronounced at 16 to 24 months.
The model was generated on a Fischer 344 background by co-injecting rat pronuclei with APPsw and PS1ΔE9 – two mutant human genes that are independent causes of early-onset familial Alzheimer’s disease, the company explained.
“We are very excited to add the TgF344-AD rat to our portfolio of mouse amyloidosis and tauopathy models. The TgF344-AD rats manifest a complete repertoire of AD pathology not fully recapitulated in comparable mouse models making it the ideal model with a high translational value to support new treatment approaches,” said Dr. Emer Leahy, president and CEO of PsychoGenics in a press release.
“Combined with our extensive capabilities including behavioral testing, neurochemistry, molecular and protein biology, electrophysiology, translational EEG, and immunohistochemistry, PGI is well positioned to evaluate important new AD treatments for our clients in this model,” he added.