In some measure, this has also been observed in vivo: treating an Alzheimer’s disease mouse model, the 5xFAD, with a mutein of NGF that behaves as a TrkA-biased agonist greatly ameliorates cognitive symptoms via a mechanism that involves microglial cells and requires the necessary modulation of important immune-related chemokines and cytokines [108]. This evidence concerns the gene NTRK1 and early-onset autosomal dominant Alzheimer disease.