Department of Neurology, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Zhengzhou, (People’s Republic of China)
In the article “TRPML1 Participates in the Progression of Alzheimer's Disease by Regulating the PPARγ/AMPK/Mtor Signalling Pathway”
[Cell Physiol Biochem 2017;43:2446-2456; DOI: 10.1159/000484449] by Zhang et al., the incorrect representative image was included in Figure 3E APP/PS1 + propranolol
as a result of an error at the time of image acquisition, the naming and saving process. The authors have re-photographed the original stained slide.
The corrected Figure 3 is shown here (see next page).
Fig. 3. TRPML1 overexpression and the inhibitors of the PPARγ/AMPK/mTOR signalling pathway rescued the memory and recognition impairments and neuronal apoptosis in mice with the APP/PS1 transgenesTRPML1 overexpression or treatment with 8-bAMP, GW9662, or propranolol caused significant reductions in the escape latency (A), travel length (B), and time across the platform (C) and markedly improved the recognition index (D) in the APP/PS1 transgenic mice compared to mice without treatment (p<0.05; n=8 in each group). (E-F) The neuronal apoptotic rate in the APP/PS1 transgenic mice with TRPML1 overexpression or treatment with 8-bAMP, GW9662 or propranolol was markedly reduced compared to that in mice without treatment (p<0.05; n=8 in each group). @p<0.05 compared to controls; #p<0.05 compared to the APP/PS1 group.