Several mechanisms have been proposed through which OS could reduce BDNF levels, including decreased CREB activity, increased NF‐κB DNA‐binding, and energy depletion [46]; and (7) finally, mitochondrial dysfunction due to Aβ as a main feature of AD is linked to differences in axonal transport of BDNF [44]. The gene discussed is NFKB1; the disease is Alzheimer disease.