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Differential impairment of spatial and nonspatial cognition in a mouse model of brain aging.
Life Sci. 2009 Jul 17; 85(3-4):127-35.LS

Abstract

AIMS

Chronic exposure to d-galactose (D-Gal), which causes acceleration in aging and simulated symptoms of natural senescence, has been used as a reliable animal model of aging. However, the different influences of D-Gal on spatial and nonspatial cognition are as yet unclear.

MAIN METHODS

In the present study, the object recognition test (ORT), object location test (OLT) and Y-maze test were carried out to assess the cognitive performance of mice after 8 weeks of chronic D-Gal exposure. The expression of oxidative-stress biomarkers in the prefrontal cortex (PFC) and caspase-3 in the hippocampus (HIP) were also determined.

KEY FINDINGS

The results of the behavioral tests indicated that after chronic D-Gal exposure, the spatial memory of mice was seriously impaired, whereas nonspatial cognition remained intact. D-Gal exposure also induced more significant changes in malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activities in the HIP than in the PFC. Furthermore, chronic D-Gal exposure triggered more substantial caspase-3 overexpression in the HIP than in the PFC.

SIGNIFICANCE

Together, these findings suggest the impairment of spatial, but not nonspatial, cognitive ability after chronic D-Gal exposure. The differential nature of this impairment might be due to the more substantial reduction of antioxidant enzyme activities and more severe neuronal apoptosis mediated by caspase-3 in the HIP. The present results also indicate that the HIP and HIP-dependent spatial cognition might be more susceptible to oxidative stress during senescence or other pathological processes.

Authors+Show Affiliations

Laboratory of Brain and Mind, Institute of Neuroinformatics, Dalian University of Technology, 116024, Dalian, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19450612

Citation

Wang, Wei, et al. "Differential Impairment of Spatial and Nonspatial Cognition in a Mouse Model of Brain Aging." Life Sciences, vol. 85, no. 3-4, 2009, pp. 127-35.
Wang W, Li S, Dong HP, et al. Differential impairment of spatial and nonspatial cognition in a mouse model of brain aging. Life Sci. 2009;85(3-4):127-35.
Wang, W., Li, S., Dong, H. P., Lv, S., & Tang, Y. Y. (2009). Differential impairment of spatial and nonspatial cognition in a mouse model of brain aging. Life Sciences, 85(3-4), 127-35. https://doi.org/10.1016/j.lfs.2009.05.003
Wang W, et al. Differential Impairment of Spatial and Nonspatial Cognition in a Mouse Model of Brain Aging. Life Sci. 2009 Jul 17;85(3-4):127-35. PubMed PMID: 19450612.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential impairment of spatial and nonspatial cognition in a mouse model of brain aging. AU - Wang,Wei, AU - Li,Song, AU - Dong,Hui-Ping, AU - Lv,Shen, AU - Tang,Yi-Yuan, Y1 - 2009/05/18/ PY - 2008/11/17/received PY - 2009/04/24/revised PY - 2009/05/03/accepted PY - 2009/5/20/entrez PY - 2009/5/20/pubmed PY - 2009/7/8/medline SP - 127 EP - 35 JF - Life sciences JO - Life Sci VL - 85 IS - 3-4 N2 - AIMS: Chronic exposure to d-galactose (D-Gal), which causes acceleration in aging and simulated symptoms of natural senescence, has been used as a reliable animal model of aging. However, the different influences of D-Gal on spatial and nonspatial cognition are as yet unclear. MAIN METHODS: In the present study, the object recognition test (ORT), object location test (OLT) and Y-maze test were carried out to assess the cognitive performance of mice after 8 weeks of chronic D-Gal exposure. The expression of oxidative-stress biomarkers in the prefrontal cortex (PFC) and caspase-3 in the hippocampus (HIP) were also determined. KEY FINDINGS: The results of the behavioral tests indicated that after chronic D-Gal exposure, the spatial memory of mice was seriously impaired, whereas nonspatial cognition remained intact. D-Gal exposure also induced more significant changes in malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activities in the HIP than in the PFC. Furthermore, chronic D-Gal exposure triggered more substantial caspase-3 overexpression in the HIP than in the PFC. SIGNIFICANCE: Together, these findings suggest the impairment of spatial, but not nonspatial, cognitive ability after chronic D-Gal exposure. The differential nature of this impairment might be due to the more substantial reduction of antioxidant enzyme activities and more severe neuronal apoptosis mediated by caspase-3 in the HIP. The present results also indicate that the HIP and HIP-dependent spatial cognition might be more susceptible to oxidative stress during senescence or other pathological processes. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/19450612/Differential_impairment_of_spatial_and_nonspatial_cognition_in_a_mouse_model_of_brain_aging_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(09)00210-0 DB - PRIME DP - Unbound Medicine ER -