Indeed, fibrillar β-amyloid, the main component of plaques in the brains of AD patients, has been shown to impair the BDNF-induced Arc expression in the cultured cortical neurons, even at low levels [21]; therefore, interfering with BDNF signaling affects the downstream neuronal functions that contribute to the development of AD [22]. The gene discussed is BDNF; the disease is Alzheimer disease.