By exploiting the human TauP301L zebrafish model, it was shown that the BDNF level was reduced and associated with axonal developmental defects, but not neuronal death, in the tauopathy condition, since exogenous BDNF supplementation was able to rescue the primary axonal growth but had no effect on Tau-induced apoptotic cells [197]. The gene discussed is MAPT; the disease is tauopathy.