Mental Stimulation, Neural Plasticity, and Aging: Directions for Nursing Research and Practice

David E. Vance, Nicole M. Webb, Janice C. Marceaux, Sarah M. Viamonte, Anne W. Foote, Karlene K. Ball


J Neurosci Nurs. 2008;40(4):241-249. 

In This Article

Neural Plasticity and Cognitive Reserve

Mental stimulation requires explicit engagement in cognitive activities with the intent to stimulate connections between neurons; as a result, the concept is closely associated with neural plasticity. Developmental theories of mental stimulation and neural plasticity in humans typically conceptualize the process as initial exposure to novel stimuli, neuronal expansion, and establishment of new "connections" between neurons (i.e., synapses). As experiences are repeated, neural pathways and connections are strengthened (i.e., learning takes place). This process probably is best summarized by the familiar phrase "Neurons that fire together wire together" (Löwell & Singer, 1992, p. 211). However, if experiences are not particularly salient or neuronal connections are not strengthened via repeated exposure, "synaptic pruning" occurs.

Diamond (1993) and other researchers further explored this concept using a rat model by systematically controlling for various components of environmental stimulation, including social interaction with other rats, exercise opportunities, and novel stimuli in the cage (e.g., toys, bridges, opportunities for exploration). This research avenue has revealed that rats exposed to more stimulating environments had increased thickness of the cerebral cortex, presumably as the result of greater and more complex neuronal pathways. Likewise, demanding mental functions in humans are presumed to require more complex neural circuitry and more dense and complex synaptic connections. Consistent with animal research, postmortem research by Arendt, Bruckner, Gertz, and Marcova (1998) noted the association between neuronal loss and premortem cognitive function in the absence of clinical dementia; in other words, neuronal loss and cognitive function are correlated even in patients who do not have dementia.

Both anatomical and neuroimaging research on neural plasticity (Stern et al., 2003; Whalley, Deary, Appleton, & Starr, 2004) have begun to clarify the construct of cognitive reserve. Cognitive reserve is believed to mediate the relationship between pathology and the onset of cognitive impairment (Stern, 2002). The importance of this hypothesis is that adults with greater cognitive reserve can sustain more neuronal loss or pathology before exhibiting signs of mild cognitive impairment or dementia. Consequently, if older adults engage in mentally stimulating activities, neural plasticity will be promoted, and, theoretically, their cognitive reserve will increase.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.