Exercising the Brain to Avoid Cognitive Decline

Examining the Evidence

William E Reichman; Alexandra J Fiocco; Nathan S Rose

Disclosures

Aging Health. 2010;6(5):565-584. 

In This Article

Brain Plasticity & Reserve Theory

Neurogenesis & Neuroplasticity

Although once considered fixed and unable to regenerate or reorganize, it is now well known that cells in the adult rodent and mammalian brain are dynamic and modifiable.[11,12] Neurogenesis is the ability of the brain to generate new cells,[11] whereas neuroplasticity refers to the capacity of the brain to change physical structure (i.e., reorganization of neuronal networks) and function in response to environmental attributes or factors.[13] The neurobiological basis for the notion that we can impact (protect or enhance) cognitive function by modifying experience is rooted in the concept of neuroplasticity.

Neuroplasticity: Evidence from Animal Models

Animal models provide a wealth of information on the neurobiological correlates of age-related brain dysfunction. Canine studies demonstrate that the brains of aged dogs accumulate Aβ, which correlates with cognitive impairment[14] and further display increased oxidative damage,[15] decreased myelination[16] and neuronal loss in the hippocampus.[17] Rodent data suggest that corticocortical circuitry deterioration may result from factors including demyelination,[18] decreased neurotransmission (e.g., N-methyl-D-aspartate receptor binding)[19] and endocrine dysregulation (e.g., of glucocorticoids or estrogen).[20,21] Finally, monkey data demonstrate age-related loss of spines on pyramidal cells and decreased density of synapses in the prefrontal cortex, all of which correlate with cognitive impairment.[22]

Initial insight into the brain's capacity of neuroplasticity stems from the plethora of animal research describing the effects that occur in the brain of the adult rodent with the provision of a more complex living environment versus a simple cage. The 'enriched environment' is a large cage that includes items such as toys, tunnels and a running wheel, all of which are considered to create cognitive stimulation. Studies show that environmentally enriched adult rodents display an increase in brain synaptic density and numbers of synapses, enlarged dendritic length, increased dendritic branching and the creation (neurogenesis) and maturation of new neurons and connections.[23,24] Presumably, several of these changes are mediated by environment-induced increases in neurotrophic factors including brain derived neurotrophic factor and nerve growth factor.[13,23] Correlated with these changes is enhancement of the rodent's motor and cognitive performance.

The effect of environmental enrichment has also been tested in transgenic mice models of AD. Following a 30-day enriched housing study, Herring and colleagues found that transgenic CRND8 mice that initially display reduced neurogenesis compared with wild-type mice exhibited enhanced cell proliferation and neurogenesis in the hippocampus.[25] Other studies have demonstrated improvements in cognitive function with reductions in Aβ plaque burden and amyloid angiopathy following enriched living,[26,27] and reductions in hyperphosphorylated tau and oligomeric Aβ, two hallmarks of AD.[28] These studies highlight the possibility that environmental enrichment, and by extension, cognitive training may be beneficial in diagnosed dementia patients by improving or stabilizing cognitive function.

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