“…8,9 For instance, the potential role of PrP in supporting axonal growth can be compensated by upregulation of integrins in PrP-knockout mice. 10 However, subsequent studies have revealed that PrP-deficient mice, after appropriate challenge, present subtle phenotypes, such as alterations in neurotransmission and synaptic plasticity, [11][12][13] hippocampal spatial memory 14 and aversive hippocampal memory in aged animals, 15 circadian rhythms 16,17 and immune responses, 18,19 as well as higher sensitivity to various stress conditions, which causes increased neuronal death. Remarkably, diverse phenotypic abnormalities were observed when PrP mutants with specific deletions in the Prnp gene were re-introduced in PrP-deficient mice.…”