Considering the role of TNC in the regulation of L-VGCCs (present data) and long-term depression (Evers et al., 2002), it is plausible to assume that a reduction in L-VGCC-dependent depression may overlap with the anti-inflammatory effects of TNC deficiency and contribute to the preservation of the postsynaptic machinery in the AD model. The gene discussed is TNC; the disease is depressive disorder.