An historic aging of the population is occurring. This unprecedented growth in the number of older adults has never been faced by humankind. In the United States, life expectancy in 1900 was 47 years; in 2006, it was 78.1 years (Heron, Hoyert, Xu, Scott, & Tejada-Vera, 2008). In 2000, the number of adults age 65 and older expected to reach 90 years of age was 28%; however, by 2050, this is expected to rise to 47%. This represents a doubling of the elderly population to 80 million. Much of this increase is due to advancements in public health, standards of living, and medical care; albeit, much of it is also due to the aging of the Baby Boomer generation, which will reach age 65 between 2010 and 2030 (Marshall, 2008).
Although the expanded life span is undoubtedly welcome, the impact on social and health care systems will be overwhelming. According to the Congressional Budget Office, by 2015, the United States is expected to spend nearly $1.8 trillion on older adults; this is expected to be nearly half of the federal budget (Haas, 2008). Given the enormity of this prospect, even small changes in helping maintain autonomy and independence may keep such societal and health care systems from being overwhelmed.
One area of particular concern is cognitive functioning. In a sample of 1,751 community-dwelling adults age 65 and older, 26% reported experiencing subjective memory loss; such complaints of memory loss corresponded to objective cognitive measures (St. John & Montgomery, 2003). In fact, such cognitive complaints often indicate future cognitive declines (Reid & Maclullich, 2006). Given the importance of cognitive functioning on performing everyday activities, such as instrumental activities of daily living (IADLs) and activities of daily living (ADLs), to remain independent (Schaie, 1996; Vance, Ball, Moore, & Benz, 2007), understanding how to promote cognitive functioning or mitigate its loss will be very important in the coming years.
The purpose of this article is to provide nurses caring for older adults with a basic understanding of the principles of positive and negative neuroplasticity and how neuroplasticity affects cognitive reserve, and subsequently cognitive and everyday functioning (Figure). Methods of facilitating positive and negative neuroplasticity, such as exercise, nutrition, and cognitive remediation, will be discussed. Finally, implications for nursing practice and research are posited.
Figure. Methods of Promoting Positive and Negative Neuroplasticity.
Nobel laureate, Santiago Ramón y Cajal, espoused that once the brain has suffered insults due to aging, injury, or disease, there is little hope of change or repair because the neuronal pathways are static. This prevailing thought kept many from exploring the potential of the brain to heal. Fortunately, scientists are becoming more aware of how malleable and plastic the brain can be (Stein, Brailowsky, & Will, 1995). In fact, the brain has the opportunity to grow and shrink due to a process called neuroplasticity.
Neuroplasticity refers to the brain’s ability to change in response to environmental stimuli (Mahncke, Bronstone, & Merzenich, 2006; Mahncke, Connor, et al., 2006). This process can best be understood through a classic experiment using the enriched environmental paradigm. In this experiment, genetically similar rats were randomly assigned to one of three environmental conditions: the enriched, the standard, and the impoverished. In the enriched environmental condition, rats were placed in a large cage with other rats. Toys and objects were also put in the cage for the rats to explore. These toys and objects were replaced periodically with new ones. In the standard environmental condition, the rats were placed in a cage with other rats; however, they had no toys or objects to explore. In the impoverished condition, the rats were placed in a cage, but in isolation.
After these rats were exposed to one of these conditions, researchers observed a number of unique outcomes. First, rats exposed to the enriched environmental condition experienced more neurological and morphological changes suggestive of better cognition than rats placed in the other two conditions. Likewise, compared with the rats in the impoverished condition, rats in the standard condition also experienced more neurological and morphological changes suggestive of better cognition. Such changes included an increase in neurotrophic growth factor, dendritic branching, and thickness of the cerebral cortex, to name just a few (Vance & Crowe, 2006).
Second, these neurological and morphological changes corresponded to better cognitive functioning. Kobayashi, Ohashi, and Ando (2002) used the enriched environmental paradigm to examine cognitive functioning in rats. After placing the rats in either the enriched or standard environment, these researchers found that when placed in a Hebb-Williams Maze Task, rats exposed to the enriched environment were able to traverse the task significantly faster than rats in the standard condition. This finding has been found with other cognitive testing, such as the Morris Water Maze (Yang et al., 2007). These results have also been found with rats of different ages, as well as rats that received chemical and surgical lesioning as a proxy of brain damage (Diamond, 1993; Paban, Jaffard, Chambon, Malafosse, & Alescio-Lautier, 2005; Puurunen & Sivenius, 2002).
These findings help formulate three principles about neuroplasticity. First, novel experiences, as approximated from the enriched environmental condition, promote positive neuroplasticity as observed by increased connections between neurons and increased markers of brain health. Second, as more connections are made between neurons, cognitive functioning is supported. This increase in connections between neurons specifically is referred to as synaptic plasticity and is characterized by a long-term change in the strength and efficacy of the contact between the pre- and post-synaptic membranes (Stein et al., 1995). In fact, more connections between the neurons means that, as they are severed due to disease, disuse, or injury, the remaining connections can reroute communication between neurons that support cognition; this is referred to as cognitive reserve (Vance & Crowe, 2006). In other words, as a basic principle, the denser the connections between the neurons, the more likely the brain will be able to function in response to insults. Third, these principles work in reverse. Just as novel experiences promote positive neuroplasticity, experiences that lack novelty and do not encourage use of existing cognitive abilities result in negative neuroplasticity, as characterized by decreased connections between neurons and reduced cognitive reserve.
These principles of positive and negative neuroplasticity can be observed in human studies as well. In a recent but well-known experiment in neuroscience, Boyke, Driemeyer, Gaser, Büchel, and May (2008) attempted to teach 69 older adults (mean age = 60, age range = 50 to 67) to juggle in a three-ball cascade pattern. Magnetic resonance imaging (MRI) was conducted before training at baseline, after training approximately 3 months after baseline, and then 3 months after training ended. Only 25 participants learned to juggle proficiently as judged by being able to do so for a minimum of 60 consecutive seconds. In these participants, analysis of the MRI scans revealed that those who learned to juggle experienced gray matter growth in the nucleus accumbens and hippocampus from baseline to their immediate posttest follow up. Given that learning to juggle is a novel experience, this finding reflects the process of positive neuroplasticity. Negative neuroplasticity was reflected in the second half of the study. An analysis of the MRI scans also revealed that those who learned to juggle but then lost the ability through disuse experienced gray matter decline in the nucleus accumbens and hippocampus from posttest follow up to 3 months after training ended.
Other studies highlight the importance of novel and challenging experiences in promoting positive neuroplasticity and cognitive reserve. In a national birth cohort, Richards, Hardy, and Wadsworth (2003) examined the impact of an active leisure life on cognitive function in later life. Controlling for confounders that could affect cognitive functioning, such as educational level, gender, occupational/social class, intelligence quotient (IQ) at adolescence, health status, and substantial mental distress, they found that spare time, leisure activities (e.g., playing cards, chess, musical instruments) were protective of cognitive functioning, specifically memory performance, at age 43. Wilson and Bennett (2003) found similar results that suggest that engaging in novel and challenging activities can be effective in promoting successful cognitive aging and may even hinder the development of Alzheimer’s disease in later life. Thus, just as physical health can be augmented through exercise and diet, neuronal and brain health can also be improved with proper mental exercise and other factors that promote positive neuroplasticity.
Promoting Positive and Negative Neuroplasticity
As the Figure highlights, there are several methods for promoting positive neuroplasticity (e.g., physical exercise); likewise, the opposite of many of these methods (e.g., sedentary behavior) discourage positive neuroplasticity and promote negative neuroplasticity. This section of the article is meant to serve as a sampling of such areas, not an exhaustive list. Yet, this article serves as a guide on how to encourage successful aging by building cognitive reserve.
Methods for promoting positive neuroplasticity include mental stimulation and intellectual pursuits, social interaction, good emotional health, physical exercise, proper nutrition, proper sleep hygiene, and cognitive remediation. As already alluded to above, engaging in novel and challenging activities, especially throughout the life span, encourages neuroplasticity by facilitating the growth of new connections between neurons. Further evidence for this comes from studies that show that those who engaged in more educational pursuits or those who played a musical instrument in an orchestra experienced a delay in dementia compared with the general population (Grant & Brody, 2004; Milan et al., 2004). These findings suggest that cognitive reserves were built that were able to compensate for the neurological insults created by age-related dementia.
Social interaction has been shown to promote positive neuroplasticity in animals; for example, rats placed in groups for 4 to 8 weeks experienced more neurogenesis in the hippocampal region of the brain compared with rats placed in isolation (Lu et al., 2003). Similarly, in their study of 1,270 older adults, Keller, Magnuson, Cernin, Stoner, and Potter (2003) observed that those who had a larger social network also had better cognitive functioning, which suggests that social interaction promotes positive neuroplasticity. Likewise, in a 4-year study of 823 older adults without dementia, Wilson et al. (2007) found that loneliness and social isolation was a risk factor for Alzheimer’s disease.
Good emotional health is also associated with good cognitive functioning (Wight, Aneshensel, Seeman, & Seeman, 2003). In a sample of 2,812 community-dwelling older adults, Bassuk, Berkman, and Wypij (1998) observed that over a period of 3 years, depressive symptomatology was predictive of cognitive declines. It appears that depression, anxiety, and other negative mood states can compromise cognitive functioning; however, treating such mood problems can ameliorate cognitive functioning.
Physiological health such as physical exercise (e.g., Lochbaum, Karoly, & Landers, 2002), proper nutrition (e.g., Solfrizzi, Panza, & Capurso, 2003), and proper sleep hygiene (e.g., Stickgold, 2005) have all been shown to improve cognitive functioning. For example, in a meta-analysis examining 18 exercise interventions conducted with older adults, Colcombe and Kramer (2003) found that those who were assigned to an aerobic exercise program and actually adhered to it for at least 6 months exhibited significant gains in memory, speed of processing, and executive functioning. Thus, promoting cognitive health translates into promoting overall physiological health, which automatically facilitates brain health.
Cognitive remediation is emerging as a distinctively designed intervention to help improve cognitive functioning in a specific area, whether it be memory, speed of processing, reasoning/executive functioning, or global cognition (Vance, Webb, et al., 2008). For example, Noice, Noice, and Staines (2004) developed Theatre Training as a cognitive intervention to improve global cognition. Recognizing that acting is an intense exercise that requires the integration of cognitive, affective, and physiological resources, these researchers assigned older adults to one of three groups: the theatre training group, a visual art group, and a no contact control group. In the theatre training group, older adults attended nine 90-minute acting lessons administered over 4 weeks. Those assigned to the visual art group simply attended a class that examined art. Researchers found that those who were involved in the theatre training improved on several cognitive measures compared with the two other groups. Such cognitive remediation interventions are also becoming computerized, which may make them more accessible to older adults who have difficulty traveling (Vance, 2008).
Methods for promoting negative neuroplasticity basically include the opposite of the methods for positive neuroplasticity, such as nonstimulating activities, social isolation, poor emotional health, sedentary lifestyle, inadequate nutrition, and inadequate sleep. All of these encourage disuse of cognitive abilities or compromise the physiological integrity of the brain. One area in particular that must be addressed is substance use. The overuse of alcohol, other drugs, or even physician-prescribed polypharmacy can negatively affect the physiological integrity of the brain, resulting in poor brain health (Myers, 2008; Rocchiccioli, Sanford, & Caplinger, 2007; Schottenbauer, Momeanan, Kerick, & Hommer, 2007).
Implications for Nursing Practice and Research
Declines in cognitive functioning increase dependence in everyday activities, such as adhering to medication regimens, remembering medical appointments, and mobility (Ball & Vance, 2007; McGuire, Ford, & Ajani, 2006; Neundorfer et al., 2004). However, maintaining cognitive health in older adults will help reduce the strain and burden on the social and health care systems. This information may be especially germane for adults who develop mild cognitive impairment and early dementia because this signals a time in which principles of positive neuroplasticity may be used (Vance, McNees, & Meneses, 2009). Therefore, out of necessity in both practice and research, nurses will become more proactive in providing and developing the tools needed to help maintain cognitive health in their older patients.
In practice, gerontological nurses will need to be vigilant concerning changes in their patients’ cognitive abilities. Documenting cognitive complaints and administering brief cognitive screens, such as the Mini-Mental State Examination (Folstein, Folstein, & McHugh, 1975), the Short Portable Mental Status Questionnaire (Fillenbaum, Landerman, & Simonsick, 1998), or any number of other standardized tests of memory or executive functioning, can help detect cognitive problems. In fact, Vance, Farr, and Struzick (2008) developed a decision tree for nurses to monitor cognitive changes in older patients with HIV to help determine when to intervene; this rubric can be readily adapted to the general older population as well. Such monitoring may also be important when patients are experiencing declines in metacognitive abilities; in other words, when they are mentally unaware that they are experiencing cognitive problems (Vance, Farr, et al., 2008). Therefore, an objective cognitive assessment or conversations with a spouse or caregiver can provide information on changes in the patient’s cognitive ability.
Gerontological nurses can also assess for factors that can contribute to cognitive complaints such as depression or substance use and refer patients for comprehensive evaluations as indicated. Likewise, gerontological nurses can provide patients with the current information on ways to maintain cognitive health. The Figure provides some of these methods, but nurse researchers will need to develop new methods and procedures for improving cognitive health in this growing population. In fact, a holistic approach may be advocated. For example, cognitive remediation may be used in conjunction with treating sleep disruptions, increasing physical exercise, and perhaps combining this with neuroleptic medications (e.g., cholinesterase inhibitors) that promote brain functioning (Keltner & Folks, 2005; Keltner, Zielinski, & Hardin, 2001; Rozzini et al., 2007). Such a holistic approach may be more advantageous than just one single method.
Furthermore, nurse researchers may develop a checklist or an assessment battery that measures and targets areas that may be addressed to promote positive neuroplasticity, reduce negative neuroplasticity, and ultimately improve cognitive health. Such an individualized approach to cognitive health has yet to be developed; however, this approach may be the most efficacious in maintaining and preserving cognitive functioning.
As the aging population grows, nurses and other allied health professionals will be increasingly confronted with the need to help older patients age successfully. Maintaining or even improving cognitive functioning is an essential component of such successful aging (Rowe & Kahn, 1997) needed to sustain autonomy and quality of life. Therefore, nurses will need to lead and collaborate in efforts with psychologists, neurologists, occupational therapists, and others versed in the cognitive sciences to develop innovative and practical strategies that are effective in improving cognitive functioning and preventing cognitive decline.
Nurses are in a unique position to help promote positive neuroplasticity because they have a great deal of direct contact with older patients who may be experiencing cognitive complaints or declines. Therefore, as educators, nurse can impart the principles of positive and negative neuroplasticity to their patients. Basically, using the metaphor that cognition is like a muscle should be a succinct didactic: Exercising your brain keeps it strong and viable, but if underused, cognitive ability atrophies.
Finally, as the empirical evidence suggests, nurses need to communicate to their younger patients that cognitive maintenance should not be considered just for the old who are experiencing cognitive complaints. Instead, methods for maintaining cognitive health throughout the life span should be encouraged to prevent cognitive decline, just as physical exercise and other health-promoting behaviors are encouraged throughout the life span to avoid health-related conditions.
- Ball, K.K. & Vance, D.E. (2007). Everyday life applications and rehabilitation of processing speed deficits: Aging as a model for clinical populations. In DeLuca, J. & Kalmar, J.H. (Eds.), Information processing speed in clinical population (pp. 243–263). New York: Taylor & Francis.
- Bassuk, S.S., Berkman, L.F. & Wypij, D. (1998). Depressive symptomatology and incident cognitive decline in an elderly community sample. Archives of General Psychiatry, 559, 1073–1081. doi:10.1001/archpsyc.55.12.1073 [CrossRef]
- Boyke, J., Driemeyer, J., Gaser, C., Büchel, C. & May, A. (2008). Training-induced brain structure changes in the elderly. Journal of Neuroscience, 28, 7031–7035. doi:10.1523/JNEUROSCI.0742-08.2008 [CrossRef]
- Colcombe, S. & Kramer, A.F. (2003). Fitness effects on the cognitive function of older adults: A meta-analytic study. Psychological Science, 14, 125–130. doi:10.1111/1467-9280.t01-1-01430 [CrossRef]
- Diamond, M. (1993). An optimistic view of the aging brain. Generations, 17, 31–33.
- Fillenbaum, G.G., Landerman, L.R. & Simonsick, E.M. (1998). Equivalence of two screens of cognitive functioning: The Short Portable Mental Status Questionnaire and the Orientation-Memory-Concentration test. Journal of the American Geriatrics Society, 46, 1512–1518.
- Folstein, M.F., Folstein, S.E. & McHugh, P.R. (1975). “Mini-mental state.” A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12, 189–198. doi:10.1016/0022-3956(75)90026-6 [CrossRef]
- Grant, M.D. & Brody, J.A. (2004). Musical experience and dementia. Hypothesis. Aging Clinical and Experimental Research, 16, 403–405.
- Haas, M.L. (2008, August). Pax American geriatrica. Miller-McCune, pp. 31–39.
- Heron, M.P., Hoyert, D.L., Xu, J., Scott, C. & Tejada-Vera, B. (2008). Deaths: Preliminary data for 2006. National Vital Statistics Reports, 56(16). Retrieved March 17, 2009, from http://www.cdc.gov/nchs/data/nvsr/nvsr56/nvsr56_16.pdf
- Keller, B.K., Magnuson, T.M., Cernin, P.A., Stoner, J.A. & Potter, J.F. (2003). The significance of social network in a geriatric assessment population. Aging Clinical and Experimental Research, 15, 512–517.
- Keltner, N. & Folks, D.G. (2005). Psychotropic drugs (4th ed.). St. Louis: Mosby.
- Keltner, N.L., Zielinski, A.L. & Hardin, M.S. (2001). Drugs used for cognitive symptoms of Alzheimer’s disease. Perspectives in Psychiatric Care, 37, 31–34.
- Kobayashi, S., Ohashi, Y. & Ando, S. (2002). Effects of enriched environments with different durations and starting times on learning capacity during aging in rats assessed by a refined procedure of the Hebb-Williams maze task. Journal of Neuroscience Research, 70, 340–346. doi:10.1002/jnr.10442 [CrossRef]
- Lochbaum, M.R., Karoly, P. & Landers, D.M. (2002). Evidence for the importance of openness to experience on performance of a fluid intelligence task by physically active and inactive participants. Research Quarterly for Exercise and Sport, 73, 437–444.
- Lu, L., Bao, G., Chen, H., Xia, P., Fan, X. & Zhang, J. et al. (2003). Modification of hippocampal neurogenesis and neuroplasticity by social environments. Experimental Neurology, 183, 600–609. doi:10.1016/S0014-4886(03)00248-6 [CrossRef]
- Mahncke, H.W., Bronstone, A. & Merzenich, M.M. (2006). Brain plasticity and functional losses in the aged: Scientific bases for novel intervention. Progress in Brain Research, 157, 81–109.
- Mahncke, H.W., Connor, B.B., Appelman, J., Ahsanuddin, O.N., Hardy, J.L. & Wood, R.A. et al. (2006). Memory enhancements in healthy older adults using a brain plasticity-based training program: A randomized, controlled study. Proceedings of the National Academy of Sciences, 103, 12523–12528. doi:10.1073/pnas.0605194103 [CrossRef]
- Marshall, V.W. (2008, January). Aging in an aging society: Brief demographic overview. Presentation at the Age in America Symposium. , Chapel Hill, NC. . Retrieved March 17, 2009, from the University of North Carolina at Chapel Hill Institute on Aging Web site: http://www.aging.unc.edu/infocenter/slides/index.html
- McGuire, L.C., Ford, E.S. & Ajani, U.A. (2006). Cognitive functioning as a predictor of functional disability in later life. American Journal of Geriatric Psychiatry, 14, 36–42. doi:10.1097/01.JGP.0000192502.10692.d6 [CrossRef]
- Milan, G., Iavarone, A., Vargas, N.F., Vargas, N.M., Fiorillo, F. & Galeone, F. et al. (2004). Effects of demographic and environmental variables on cognitive performance in a rural community sample of elderly people living in southern Italy. Aging Clinical and Experimental Research, 16, 398–402.
- Myers, J.S. (2008). Factors associated with changing cognitive function in older adults: Implications for nursing rehabilitation. Rehabilitation Nursing, 33, 117–123.
- Neundorfer, M.M., Camp, C.J., Lee, M.M., Skrajner, M.J., Malone, M.L. & Carr, J.R. (2004). Compensating for cognitive deficits in persons aged 50 and over with HIV/AIDS: A pilot study of a cognitive intervention. Journal of HIV/AIDS and Social Services, 3(1), 79–97. doi:10.1300/J187v03n01_07 [CrossRef]
- Noice, H., Noice, T. & Staines, G. (2004). A short-term intervention to enhance cognitive and affective functioning in older adults. Journal of Aging and Health, 16, 562–585. doi:10.1177/0898264304265819 [CrossRef]
- Paban, V., Jaffard, M., Chambon, C., Malafosse, M. & Alescio-Lautier, B. (2005). Time course of behavioral changes following basal forebrain cholinergic damage in rats: Environmental enrichment as a therapeutic intervention. Neuroscience, 132, 13–32. doi:10.1016/j.neuroscience.2004.11.024 [CrossRef]
- Puurunen, K. & Sivenius, J. (2002). Influence of enriched environment on spatial learning following cerebral insult. Reviews in the Neurosciences, 13, 347–364.
- Reid, L.M. & Maclullich, A.M. (2006). Subjective memory complaints and cognitive impairment in older people. Dementia and Geriatric Cognitive Disorders, 22, 471–485. doi:10.1159/000096295 [CrossRef]
- Richards, M., Hardy, R. & Wadsworth, M.E. (2003). Does active leisure protect cognition? Evidence from a national birth cohort. Social Science & Medicine, 56, 785–792. doi:10.1016/S0277-9536(02)00075-8 [CrossRef]
- Rocchiccioli, J.T., Sanford, J. & Caplinger, B. (2007). Polymedicine and aging: Enhancing older adult care through advanced practitioners. Journal of Gerontological Nursing, 33(7), 19–24.
- Rowe, J.W. & Kahn, R.L. (1997). Successful aging. The Gerontologist, 37, 433–440.
- Rozzini, L., Costardi, D., Chilovi, B.V., Franzoni, S., Trabucchi, M. & Padovani, A. (2007). Efficacy of cognitive rehabilitation in patients with mild cognitive impairment with cholinesterase inhibitors. International Journal of Geriatric Psychiatry, 22, 356–360. doi:10.1002/gps.1681 [CrossRef]
- Schaie, K.W. (1996). Intellectual development in adulthood: The Seattle Longitudinal study. New York: Cambridge University Press.
- Schottenbauer, M.A., Momenan, R., Kerick, M. & Hommer, D.W. (2007). Relationships among aging, IQ, and intracranial volume in alcoholics and control subjects. Neuropsychology, 21, 337–345. doi:10.1037/0894-422.214.171.1247 [CrossRef]
- Solfrizzi, V., Panza, F. & Capurso, A. (2003). The role of diet in cognitive decline. Journal of Neural Transmission, 110, 95–110.
- Stein, D.G., Brailowsky, S. & Will, B. (1995). Brain repair. New York: Oxford University Press.
- Stickgold, R. (2005). Sleep-dependent memory consolidation. Nature, 437, 1272–1278. doi:10.1038/nature04286 [CrossRef]
- St. John, P. & Montgomery, P. (2003). Is subjective memory loss correlated with MMSE scores or dementia?Journal of Geriatric Psychiatry and Neurology, 16, 80–83. doi:10.1177/0891988703016002003 [CrossRef]
- Vance, D.E. (2008). Training the brain: Cognitive remediation therapy has applications for long-term care settings. Advance for Directors in Rehabilitation, 17(11), 33–34, 36.
- Vance, D.E., Ball, K.K., Moore, B.S. & Benz, R.L. (2007). Cognitive remediation therapies for older adults: Implications for nursing practice and research. Journal of Neuroscience Nursing, 39, 226–231. doi:10.1097/01376517-200708000-00007 [CrossRef]
- Vance, D.E. & Crowe, M. (2006). A proposed model of neuroplasticity and cognitive reserve in older adults. Activities, Adaptation, & Aging, 30(3), 61–79. doi:10.1300/J016v30n03_04 [CrossRef]
- Vance, D.E., Farr, K. & Struzick, T.C. (2008). Assessing the clinical value of cognitive appraisal in adults aging with HIV. Journal of Gerontological Nursing, 34(1), 36–41. doi:10.3928/00989134-20080101-11 [CrossRef]
- Vance, D.E., McNees, P. & Meneses, K. (2009). Technology, cognitive remediation, and nursing: Directions for successful cognitive aging. Journal of Gerontological Nursing, 35(2), 50–56. doi:10.3928/00989134-20090201-09 [CrossRef]
- Vance, D.E., Webb, N.M., Marceaux, J.C., Viamonte, S.M., Foote, A.W. & Ball, K.K. (2008). Mental stimulation, neural plasticity, and aging: Directions for nursing research and practice. Journal of Neuroscience Nursing, 40, 241–249. doi:10.1097/01376517-200808000-00008 [CrossRef]
- Wight, R.G., Aneshensel, C.S., Seeman, M. & Seeman, T.E. (2003). Late life cognition among men: A life course perspective on psychosocial experience. Archives of Gerontology and Geriatrics, 37, 173–193. doi:10.1016/S0167-4943(03)00046-3 [CrossRef]
- Wilson, R.S. & Bennett, D.A. (2003). Cognitive activity and risk of Alzheimer’s disease. Current Directions in Psychological Science, 12(3), 87–91. doi:10.1111/1467-8721.01236 [CrossRef]
- Wilson, R.S., Krueger, K.R., Arnold, S.E., Schneider, J.A., Kelly, J.F. & Barnes, L.L. et al. (2007). Loneliness and risk of Alzheimer’s disease. Archives of General Psychiatry, 64, 234–240. doi:10.1001/archpsyc.64.2.234 [CrossRef]
- Yang, J., Hou, C., Ma, N., Liu, J., Zhang, Y. & Zhou, J. et al. (2007). Enriched environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress. Neurobiology of Learning and Memory, 87, 257–263. doi:10.1016/j.nlm.2006.09.001 [CrossRef]