Darkthorn’s Blog

Increase in the human life-span is creating a need to maintain physical and cognitive function into old age to reduce the need for assistance in older adults’ lives. A study by Access Economics for Alzheimer’s Australia, estimated that dementia and Alzheimer’s disease touched the lives of at least 2.3 million Australians in 2003. The primary carers, mainly family and friends of the patient, save the economy $16 billion annually by providing support within their own homes (Access Economics, 2003).

A number of lifestyle factors, such as intellectual activity, social interaction, diet and physical activity are all associated with the maintenance of cognitive function, as well as a reduction in risk for neurodegenerative disorders (Vaynman & Gomez-Pinilla, 2006; Karp, 2006; Themanson & Hillman, 2006).

Diet and Nutrition

The elderly are at high risk of nutritional deficiency because of altered taste or smell (and therefore reduced appetite), impaired digestion or absorption of nutrients (due to chronic disease or drug-nutrient interference) and also a limited range of food choices (brought about by less mobility, lower income, and declining health) (Gillette-Guyonnet et al., 2007).

Although benefits from nutritional changes have been investigated, it is difficult to evaluate clinically the effect of diet on maintenance of cognitive function (Milgram et al., 2006). This is because of flawed study conditions, such as lack of statistical control, minimal control of other contribution factors and participant selection bias (Gillette-Guyonnet et al., 2007). However, deficiencies of nutrients are shown overall to have a negative effect on maintaining cognitive function.

Vitamin B

Vitamin B12 deficiencies, as well as lowered folate levels are common in the elderly (de Groot et al., 2004). Studies suggest that the B vitamin (especially B9 and B12) has a protective effect against cognitive decline. Although no official conclusions have been drawn, a slight correlation between vitamin B deficiencies and cognitive decline is apparent, due to the role it plays in the methylation processes essential for brain function (Gillette-Guyonnet et al., 2007).

Antioxidants

Zinc and selenium play an important role in cellular maintenance within the body, including replication, cell respiration and free radical elimination (Savarino et al., 2001). Deficiencies of either of these antioxidants can impact on the aging process.

The effects of zinc on cognitive function (as measured by visual and working memory, attention and reaction time) were examined by Maylor et al. (2006). A healthy sample of adults who had supplements of zinc (30 mg/d) over 3 months was found to have an improved memory and attention (Maylor et al., 2006). These findings could not be generalised to include older adults in poorer mental health however, nor was the study longitudinal to examine the long-term effect of zinc supplements.

When selenium deficiency is present in healthy subjects (greater than 90 years), there is a correlation with higher mortality rate (Savarino et al., 2001). Savarino et al. (2001) suggests that monitoring selenium and zinc levels may also be an effective way of detecting early signs of disease.

Fatty Acids

The research into the role of fatty acids in influencing cognitive decline is inconclusive and contradictive. Gillette-Guyonnet et al. (2007) hypothesises that this is because of the varying lengths of the studies. Overall, it can be tentatively concluded that a high intake of saturated and trans-unsaturated fatty acids contributes towards increased risk of Alzheimer’s disease, whilst polyunsaturated and monounsaturated fats do not (Gillette-Guyonnet et al., 2007).

Fish

Unsurprisingly, regular fish consumption (once or twice a week) promotes a lower risk of Alzheimer’s disease.  Current clinical trials involve the use of n-3 PUFA to eliminate cross-contaminants and create a more stable basis for results (how much n-3 PUFA is optimal for reducing the risk of dementia) (Gillette-Guyonnet et al., 2007).

Physical Exercise

Older adults who regularly performed physical activities had a higher functional cognitive rate than their sedentary peers (Hillman, Erickson & Kramer, 2008). Research has also shown a positive correlation between aerobic fitness and academic achievement in school-age children (California Department of Education, 2001, as cited in Hillman, Erickson & Kramer, 2008), although further research is required to ascertain the effects of exercise over the entire lifespan.

Animal research, such as that done by Vaynman and Gomez-Pinilla (2006), has shown that exercise has a positive effect on neuronal processes and growth (especially synaptic plasticity and neuronal cell survival), showing the correlation between active behaviours and supporting brain structures. Vaynman and Gomez-Pinilla suggest that the sedentary lifestyle and eating behaviours are impacting negatively on human health, with a rise of metabolic disorders across the entire population.

Studies by Sherwood and Selder (1979), Spirduso (1975) and Spirduso and Clifford (1978) indicated that intensive cardio-respiratory training had a positive impact on maintaining reaction time in older adults. A more recent study by Themanson and Hillman (2006) indicated that cardio-respiratory fitness, but not acute aerobic exercise increases top-down attentional control. In all studies, physical activity had a positive effect on cognition.

Although various cognitive processes benefit from physical activity, some are more obviously influenced. Executive control (attentional resources and cognitive processing) is comparatively better protected than other processes by exercise (Hillman, Erickson & Kramer, 2008).

The mixed pattern of results obtained across studies may be accounted for by the cognitive facets examined, the type of exercise program and the methods of observing fitness improvements (Hillman, Erickson & Kramer, 2008). The confounding variables, such as age, education and race were also not taken into account in several studies, further compromising the results (Hillman, Erickson & Kramer, 2008).

Cognitive Exercise

An early exposure to cognitive exercise and enrichment activity (such as education, work environment characteristics, leisure activity complexity and specific cognitive training) appears to protect against age-related cognitive decline and the common neurodegenerative disorder, dementia (Milgram et al., 2006).

Education

Levels of education have an inversely proportional relationship with the likelihood of dementia development (Wilson et al., 2002, as cited in Milgram et al., 2006). Mental vitality, verbal and non-verbal memory and conceptualisation are also positively affected by higher levels of education (Butler et al., 1996; Albert et al., 1995). High levels of linguistic ability, nurtured by education at an early age, are shown to be associated with lower cognitive impairment and less symptoms of Alzheimer’s disease later in life (Riley et al., 2005).

Work Complexity

The complexity of work, as defined by requirements of thought and independent judgement, also has a positive effect on cognitive performance and maintenance at an older age (Mulatu & Schooler, 1999). Mulatu and Schooler (1999) also looked at the psychological and socio-demographic characteristics of participants, and concluded that these were good predictors of cognitive health, having effects on performance even after 20 years.

Leisure Activity

Wilson et al. (2002, as cited in Milgram et al., 2006) looked at seven measures of leisure activity and discovered that the risk of developing Alzheimer’s disease was reduced when the activities were more complex.

Cognitive Training

Although specific cognitive training has an overall positive effect on attention, generally only the specific function targeted by the training is noticeably different in performance levels (Milgram et al., 2006).

Neurobiological Correlations

Anderson and Grady (2001, as cited in Milgram et al., 2006) found that in older subjects, the overall increase in cerebral blood flow is less than in younger subjects, but the spatial extent of activation is greater. These results, from a set of normal older adults, showed that aging is naturally associated with functional reorganization, which provides support for the cognitive aging reserve hypothesis (Milgram et al., 2006).

Animal studies, mainly in rats, have shown an increase in magnitude of hippocampal depth (endothelial cell proliferation) when exposed to stimulating environments (Ekstrand, Hellsten & Tingstro?m, 2008). This same study suggests that raised cortisol concentrations in older patients (such as is produced by high stress levels) may lead to reduction in endothelial cell formation, and corresponding impaired mental function (Ekstrand et al., 2008)

Hypotheses

Brain reserve, as determined by pre-cognitive decline neuronal numbers and level of neuronal compensation (the use of different brain networks in place of damaged structures), is the threshold of brain damage that can be sustained (for a given individual) before symptoms of decline are clinically noticeable (Stern. Y., 2006, as cited in Galluzi et al., 2008). The ‘Cognitive Aging Reserve Hypothesis’ concludes that this neuroplasiticity is linked to environmental (experience and drugs) and biological (eg. neurogenesis and synaptic sprouting) factors, enabling normal cognitive function despite the presence of brain pathology (Galluzzi et al., 2008).

An alternative hypothesis, the ‘Disuse Hypothesis of Cognitive Aging’, assigns the loss of fluid intelligence to reduced cognitive exercise (such as that brought about by retirement) (Tranter & Koutstaal, 2008). By providing stimulating mental exercises to determine the relationship with positive changes in problem solving and flexible thinking performance, Tranter & Koutstaal (2008) concluded that even within a short time span (10-12 weeks), fluid intelligence could be significantly improved by cognitive exercise.

Other Factors

Social Networks

A comprehensive large scale study (n = 1473) by Fratiglioni et al. (2000) found that participating in social activities and having close social ties with family and friends provided protection from dementia, even after taking into account variables such as age, sex, education, and initial cognitive level. Karp et al. (2006) concluded, at the completion of a three year study, that cognitive, social and physical engagement all served to decrease the risk of dementia. The study examined leisure activities carried out by older adults as a complex measure of all three areas (Karp et al., 2006).

Inflammation

Eriksson et al. (2008) found that atopic disorders such as asthma, eczema and rhinitis were associated with an increased risk of Alzheimer’s disease, while an asthma history indicated a shorter life expectancy after diagnosis. The use of the twin study method minimised genetic and environmental confounds.

Genetics

The ApoE gene, as well as the GAB2 gene, increases the risk of developing Alzheimer’s Disease, but are not definitive determinates (Albert, 1996). Although increased risk is associated with two copies of the ApoE 4 allele or ApoE 3,4 genotype, having these genes does not always result in the development of Alzheimer’s Disease, indicating the influence of many environmental factors (Albert, 1996).

Although very little can be done to change genetics, being able to identify elderly people most at risk of developing Alzheimer’s Disease will make early intervention measures (such as increased exercise or cognitive activities) more effective at preventing dementia from rapidly progressing.

Conclusion

In most studies, it was found that although cognitive function improved with application of physical or mental exercise or dietary changes, it was difficult to ascertain the level of benefit obtained. Research into education and work complexity earlier in life generally showed results that showed an increase in relative cognitive function in older adults, but was inconclusive as to when applying cognitive exercise would be most beneficial in maintaining function. Studies indicated that exercise in each stage of life had a positive effect on cognitive function within the time frame of the study, but further longitudinal studies would provide a more informative basis for the effects of exercise across the entire human lifespan.

References

Access Economics (2003). The Dementia Epidemic: Economic Impact and Positive Solutions for Australia. Retrieved August 29, 2008 from http://www.alzheimers.org.au/upload/EpidemicFullReportMarch2003.pdf

Albert, M.S. et al. (1995). Predictors of cognitive change in older persons. Psychol. Aging, 10, 578-589.

Albert, M. S. (1996). Cognitive and neurobiologic markers of early Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America, 93, 13547-13551.

Butler, S.M., Ashford, J.W., & Snowdon, D.A. (1996). Age, education and changes in the mini-mental state exam scores of older women: findings from the Nun Study. J. Am. Geratric. Soc. 44, 675-681.

Ekstrand, J., Hellsten, J., & Tingstro?m, A. (2008). Environmental enrichment, exercise and corticosterone affect endothelial cell proliferation in adult rat hippocampus and prefrontal cortex. Neuroscience Letters, 442 (3), 203-207.

Eriksson, U.K. et al. (2008). Asthma, Eczema, Rhinitis and the Risk for Dementia. Dementia and geriatric cognitive disorders, 25 (2), 148.

Fratiglioni, L., Wang, H.X., Ericsson, K., Maytan, M. & Winblad, B. (2000). Influence of social network on occurrence of dementia: a community-based longitudinal study. Lancet, 355, 1315-1319.

de Groot, L., Verheijden, M.W., de Henauw, S. et al. (2004). Life style, nutritional status, health, and mortality in elderly people across Europe: a review of the longitudinal results of the SENECA study. J. Gerontology Med. Sci., 59A (12), 1277-1285.

Galluzzi, S., Lanni, C., Pantoni, L., Filippi, M., & Frisoni, G.B. (2008). White matter lesions in the elderly: Pathophysiological hypothesis on the effect on brain plasticity and reserve. Journal of the Neurological Sciences, 273 (1-2), 3-9.

Gillette-Guyonnet, S., Abellan Van Kan, G., Andrieu, S., Barberger-Gateau, P. et al. (2007). INNA task force on nutrition and cognitive decline with aging. Journal of Nutrition, Health & Aging, 11,132-152.

Hillman, C. H., Erickson, K. I., & Kramer, A. F. (2008). Be smart, exercise your heart: exercise effects on brain and cognition. Nature Reviews: Neuroscience, 9, 58-65.

Karp, A. et al. (2006). Mental, physical, and social components in leisure activities equally contribute to decrease dementia risk. Dement. Geriat. Cogn. Disord. 21, 65-73.

Maylor, E.A. et al. (2006). Effects of zinc supplementation on cognitive function in healthy middle-aged and older adults: The ZENITH study. British Journal of Nutrition, 96 (4), 752-760.

Milgram, N. W., Siwak-Tapp, C. T., Araujo, J., & Head, E. (2006). Neuroprotective effects of cognitive enrichment. Ageing Research Reviews, 5, 345-369.

Mulatu, M. S. & Schooler, C. (1999). Longitudinal effects of occupational, psychological, and social background characteristics on health of older workers. Ann. NY Acad. Sci., 896, 406-408.

Riley, K.P., Snowdon, D. A., Desrosiers M.F., & Markesbery, W.R. (2005). Early life linguistic ability, late life cognitive function, and neuropathology: findings from the Nun Study, Neurobiol. Aging, 26, 341-347.

Savarino, L. et al. (2001). Serum concentrations of zinc and selenium in elderly people: Results in healthy nonagenarians/centenarians. Experimental Gerontology, 36 (2), 327-339.

Sherwood, D. E. & Selder, D. J. (1979). Cardiorespiratory health, reaction time and aging. Med. Sci. Sports, 11, 186-189.

Spirduso, W. W. (1975). Reaction and movement time as a function of age and physical activity level. J. Gerontol. 30, 435-440.

Spirduso, W. W. & Clifford, P. (1978). Replication of age and physical activity effects on reaction and movement times. J. Gerontol. 33, 26-30.

Themanson, J. R. & Hillman, C. H. (2006). Cardiorespiratory fitness and acute aerobic exercise effects on neuroelectric and behavioral measures of action monitoring. Neurosci. 141, 757-767.

Tranter, L. J., & Koutstaal, W. (2008). Age and flexible thinking: An experimental demonstration of the beneficial effects of increased cognitively stimulating activity on fluid intelligence in healthy older adults. Aging, Neuropsychology and Cognition, 15, 184-207.

Vaynman, S. & Gomez-Pinilla, F. (2006). Revenge of the “sit”: how lifestyle impacts neuronal and cognitive health though molecular systems that interface energy metabolism with neuronal plasticity. J. Neurosci. Res. 84, 699-715.