The same group showed in vivo that in a non-transgenic animal model of Alzheimer’s disease, induced by intracerebroventricular (i.c.v.)Aβ1–42 administration in rat, the prokineticin system is strongly upregulated in neurons and astrocytes of the hippocampus [43] and that pharmacological blockade of prokineticin receptors with PC1 protects against Aβ1–42 induced cognitive deficits by reducing the overexpression of PK2 and PKRs. Here, PROK2 is linked to early-onset autosomal dominant Alzheimer disease.