Open Access

An enriched environment delays the progression from mild cognitive impairment to Alzheimer's disease in senescence‑accelerated mouse prone 8 mice

  • Authors:
    • Jian-Zhong Li
    • Xing-Hua Hao
    • Hai-Ping Wu
    • Ming Li
    • Xue-Min Liu
    • Zhi-Bing Wu
  • View Affiliations

  • Published online on: September 20, 2021     https://doi.org/10.3892/etm.2021.10755
  • Article Number: 1320
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

A previous study demonstrated that middle‑aged (5‑6 months of age) senescence‑accelerated mouse prone 8 (SAMP8) mice can be used as animal models of mild cognitive impairment (MCI). An enriched environment (EE) can mitigate cognitive decline and decrease the pathological changes associated with various neurodegenerative diseases. In the present study, the learning‑memory abilities of SAMP8 mice during the MCI phase (5 months of age) was evaluated and neuropathological changes in the hippocampus were examined after the mice were exposed to an EE for 60 days. In the Morris water maze test, EE‑exposed mice demonstrated significantly decreased escape latency and increased time spent in the target quadrant and number of platform crossings compared with control mice. Terminal deoxynucleotidyl transferase dUTP nick end labeling and Nissl staining showed that EE‑exposed mice had reduced neuronal apoptosis and increased number of surviving neurons compared with control mice. Golgi staining, transmission electron microscopy, and immunohistochemical staining demonstrated that EE‑exposed mice exhibited increased dendritic spine densities among secondary and tertiary apical dendrites; increases in synaptic numerical density, synaptic surface density, and expression of synaptophysin; and reduced deposition of amyloid‑β (Aβ) and expression of amyloid‑precursor protein (APP) in the hippocampal CA1 region compared with control mice. These results demonstrate that EE exposure effectively decreases neuronal loss and regulates neuronal synaptic plasticity by reducing the expression of APP and the deposition of Aβ in the hippocampal CA1 region, thereby mitigating cognitive decline in SAMP8 mice during the MCI phase and delaying the progression from MCI to Alzheimer's disease.
View Figures
View References

Related Articles

Journal Cover

November-2021
Volume 22 Issue 5

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li J, Hao X, Wu H, Li M, Liu X and Wu Z: An enriched environment delays the progression from mild cognitive impairment to Alzheimer's disease in senescence‑accelerated mouse prone 8 mice. Exp Ther Med 22: 1320, 2021
APA
Li, J., Hao, X., Wu, H., Li, M., Liu, X., & Wu, Z. (2021). An enriched environment delays the progression from mild cognitive impairment to Alzheimer's disease in senescence‑accelerated mouse prone 8 mice. Experimental and Therapeutic Medicine, 22, 1320. https://doi.org/10.3892/etm.2021.10755
MLA
Li, J., Hao, X., Wu, H., Li, M., Liu, X., Wu, Z."An enriched environment delays the progression from mild cognitive impairment to Alzheimer's disease in senescence‑accelerated mouse prone 8 mice". Experimental and Therapeutic Medicine 22.5 (2021): 1320.
Chicago
Li, J., Hao, X., Wu, H., Li, M., Liu, X., Wu, Z."An enriched environment delays the progression from mild cognitive impairment to Alzheimer's disease in senescence‑accelerated mouse prone 8 mice". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1320. https://doi.org/10.3892/etm.2021.10755