Correction: Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model

In the second panel of the IBA1 micrographs in Fig. 2e, the animal from the APN-βA was repeated instead of employing the corresponding representative section for the APN group, now the group has been corrected. In the second panel of the IBA1 micrographs in Fig. 2e, the animal from the APN-βA was repeated instead of employing the corresponding representative section for the APN group, now the group has been corrected. Fig. 2 figure 2 Immunohistological determination of NeuN and Iba-1 expression in the olfactory bulb. a Representative micrographies of the olfactory bulb showing the evaluated areas for NeuN and Iba‐1, scale bar 250 μm; the arrows denote the region where glomeruli are disarranged. b Representative micrographies of NeuN (top) and Iba‐1 (bottom) of the granular cell layer (GCL) with examples of the random squares (ROIs) quantified, scale bars 50 μm. c Number of NeuN expressing cells in the GCL for Vehicles (VEH), adiponectin (APN), Amyloid‐β (Aβ) and APN-Aβ injected rats (F[3, 20] = 0.1, p < 0.94). d Number of Iba‐1 positive cells per area of the GCL of the same groups (F[3, 20] = 0.6336, p < 0.602). e Representative micrographies of the glomeruli with examples of the random squares (ROIs) quantified, scale bar 50 μm. f Number of NeuN expressing cells in the glomeruli per area of the same groups (F[3, 68] = 15.93, p < 0.0001). g Number of Iba‐1 positive cells per area (F[3, 20] = 0.7029, p < 0.5614.