Abstract:
Tg(5XFAD)/B-hTFR1 mice were obtained by mating Tg(5XFAD) mice B-hTFR1 mice. These mice began to exhibit Aβ plaques at 2 months and were exacerbated by age. Soluble and insoluble Aβ40 and Aβ42 are elevated in the brain with an age-dependent fashion. The female mice exhibited deficits in spatial learning and memory by 6 months. Trontinemab analog can rapidly and markedly reduce Aβ plaques and reverse behavioral impairments. These mice provide a reliable preclinical model for the development and efficacy testing of AD therapeutics that leverage TFR1 targeting for enhanced brain penetration.
