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Dl‑3‑n‑butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal‑enriched protein tyrosine phosphatase/ERK/cAMP‑response element‑binding protein signaling pathway

Corrigendum in: /10.3892/etm.2022.11742

  • Authors:
    • Yan Zhao
    • Wen-Qiang Yang
    • Lu Yu
    • Jing Yang
    • Hai-Rong Zhu
    • Lin Zhang
  • View Affiliations

  • Published online on: March 10, 2022     https://doi.org/10.3892/etm.2022.11248
  • Article Number: 319
  • Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and the deposition of amyloid plaques in the brain. In a transgenic mouse model of AD, cognitive impairment and synaptic dysfunction were revealed to be associated with soluble amyloid oligomers and to occur prior to plaque formation. The results of our previous studies revealed that striatal‑enriched protein tyrosine phosphatase (STEP)61 negatively regulated the β‑amyloid protein‑mediated ERK/cAMP‑response element‑binding protein (CREB) signaling pathway. Dl‑3‑n‑butylphthalide (NBP) is a synthetic compound approved by the Food and Drug Administration of China for the treatment of ischemic stroke in 2002. Studies have shown that the neuroprotective effects of NBP involve multiple mechanisms. The present study further explored the mechanism of NBP therapy in amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mice, and the involvement of the STEP/ERK/CREB signaling pathway. The results suggested that NBP treatment effectively ameliorated the spatial learning and memory impairment of the APP/PS1 transgenic mice, which was assessed using a Morris water maze. In addition, NBP reduced amyloid‑induced activation of STEP61 levels, while increasing phosphorylated (p)‑ERK1/2 and p‑CREB levels in the cerebral cortex and hippocampus of APP/PS1 transgenic mice by western blotting and immunostaining. In conclusion, the present study provided evidence to suggest that the new drug NBP improved amyloid‑induced learning and memory deficits, likely through the regulation of the STEP/ERK/CREB pathway. The results revealed that NBP, as a multi‑target drug, may exert a neuroprotective effect. Therefore, NBP may serve as an effective treatment for AD.
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May-2022
Volume 23 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhao Y, Yang W, Yu L, Yang J, Zhu H and Zhang L: Dl‑3‑n‑butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal‑enriched protein tyrosine phosphatase/ERK/cAMP‑response element‑binding protein signaling pathway Corrigendum in /10.3892/etm.2022.11742. Exp Ther Med 23: 319, 2022
APA
Zhao, Y., Yang, W., Yu, L., Yang, J., Zhu, H., & Zhang, L. (2022). Dl‑3‑n‑butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal‑enriched protein tyrosine phosphatase/ERK/cAMP‑response element‑binding protein signaling pathway Corrigendum in /10.3892/etm.2022.11742. Experimental and Therapeutic Medicine, 23, 319. https://doi.org/10.3892/etm.2022.11248
MLA
Zhao, Y., Yang, W., Yu, L., Yang, J., Zhu, H., Zhang, L."Dl‑3‑n‑butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal‑enriched protein tyrosine phosphatase/ERK/cAMP‑response element‑binding protein signaling pathway Corrigendum in /10.3892/etm.2022.11742". Experimental and Therapeutic Medicine 23.5 (2022): 319.
Chicago
Zhao, Y., Yang, W., Yu, L., Yang, J., Zhu, H., Zhang, L."Dl‑3‑n‑butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal‑enriched protein tyrosine phosphatase/ERK/cAMP‑response element‑binding protein signaling pathway Corrigendum in /10.3892/etm.2022.11742". Experimental and Therapeutic Medicine 23, no. 5 (2022): 319. https://doi.org/10.3892/etm.2022.11248