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. 2019 Dec 31;143(3):e23. doi: 10.1093/brain/awz409

Corrigendum

PMCID: PMC7089655  PMID: 31891369

Christopher D. Morrone, Paolo Bazzigaluppi, Tina L. Beckett, Mary E. Hill, Margaret M. Koletar, Bojana Stefanovic and JoAnne McLaurin. Regional differences in Alzheimer’s disease pathology confound behavioural rescue after amyloid-β attenuation. Brain 2020; 143: 359–373. doi:10.1093/brain/awz371.

The author apologizes for an error in the y-axes of Fig. 5B, D and F.

This has been corrected.

Figure 5.

Figure 5

Amyloid-β attenuation decreases tau pathology in a brain region-dependent manner. Tau pathology was assessed in TgF344-AD rats (Tg, Tg-SI) by immunostaining with PHF1 to label hyperphosphorylated tau at S396/404 and Thioflavin-S (Thio-S) to label amyloid-β plaques. (A) PHF1+/Thio-S+ staining in the dentate gyrus (DG) of a Tg rat. Approximately 80–85% of PHF1+ inclusions (red) associate with amyloid-β plaques (green), representing dystrophic neurites. [A(i)] The remainder of the tau inclusions are non-plaque associated, representing pretangle inclusions. (B) PHF1+ inclusions were separated into plaque and non-plaque associated, and quantified by immunohistochemistry (Supplementary Fig. 7) in the dentate gyrus. Amyloid-β attenuation significantly decreased plaque-associated, but not non-plaque associated inclusions. [C and C(i)] PHF1+/Thio-S+ staining in the entorhinal cortex of a Tg rat indicating plaque-associated inclusions and non-plaque associated inclusions. (D) There was no effect of treatment on either plaque-associated or non-plaque associated inclusions in the entorhinal cortex (EC) (E), despite a reduction of amyloid-β plaques in the region. (F) No significant differences were detected in the number of total entorhinal cortical neurons across genotype and treatment (G); however, Tg and Tg-SI rats exhibit a decrease of neurons within layer II of the entorhinal cortex. Scale bars = 20 μm in A and C; 10 μm in A(i) and C(i). n = 6, mean ± SEM, two-sided unpaired t-test, ***P < 0.001.


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