Lifelong environmental enrichment in the absence of exercise protects the brain from age-related cognitive decline

Abstract

ABSTRACT Environmental manipulations enhance neuroplasticity, with enrichment‐induced cognitive improvements linked to increased expression of growth factors and enhanced hippocampal neurogenesis. Environmental enrichment (EE) is defined as the addition of social, physical and somatosensory stimulation into an animal s environment via larger group housing, extra objects and, often, running wheels. Previous studies from our laboratory report that physical activity is a potent memory enhancer but that long‐term environmental stimulation can be as effective as exercise at ameliorating age‐related memory decline. To assess the effects of EE, in the absence of exercise, rats were housed in continuous enriched conditions for 20 months and memory assessed at young, middle aged and aged timepoints. MRI scans were also performed at these timepoints to assess regional changes in grey matter and blood flow with age, and effects of EE upon these measures. Results show an age‐related decline in recognition, spatial and working memory that was prevented by EE. A parallel reduction in &bgr;NGF in hippocampus, and cell proliferation in the dentate gyrus, was prevented by EE. Furthermore, EE attenuated an age‐related increase in apoptosis and expression of pro‐inflammatory markers IL‐1&bgr; and CD68. Long‐term EE induced region‐specific changes in grey matter intensity and partially rescued age‐related reductions in cerebral blood flow. This study demonstrates that sensory enrichment alone can ameliorate many features typical of the ageing brain, such as increases in apoptosis and pro‐inflammatory markers. Furthermore, we provide novel data on enrichment‐induced regional grey matter alterations and age‐related changes in blood flow in the rat. This article is part of the Special Issue entitled “Neurobiology of Environmental Enrichment”. HighlightsEnvironmental enrichment without exercise (EE) prevents age‐related decline in cognition.EE prevents age‐related decline in spatial and recognition memory.EE prevents an age‐related decrease in cell proliferation in the dentate gyrus.EE prevents an age‐related increase in apoptosis and inflammation in the dentate gyrus.