13 November, 2017

Dementia will become more common as our population ages. Globally, 15 million people were affected by dementia in 2015 and this number is expected to triple by 2050. Reduced exposure to dementia risk factors and increased exposure to protective factors create a 'cognitive buffer', reducing the progression to, or delaying the onset of, dementia.

It is thought that more than one-third of dementia cases may be preventable by modifying nine lifestyle factors. It has recently been suggested by the Lancet Commission on Dementia Prevention, Intervention and Care that, even if there is a genetic tendency for dementia, addressing these nine factors across the lifespan is associated with a reduced risk of dementia in later life [1]. There is no disease-modifying treatment for any common dementia, so delaying the onset of dementia would be of great benefit to the individual, their families and supporters, as well as the general community.

The potentially modifiable risk factors are:

• not completing secondary education in early life (under 18 years old),
• high blood pressure, obesity and hearing loss in midlife (age 45-65 years),
• smoking, depression, physical inactivity, social isolation, and diabetes in later life (greater than 65 years).

The brain mechanisms thought to provide preventive strategies incorporate:

1. Increasing brain reserve by preserving hearing, early life education, cognitive training, reducing depression, exercising and having a rich social network;
2. Reducing brain damage (vascular, neurotoxic) by reducing obesity, depression, treating diabetes, high blood pressure, and high cholesterol, exercising, having a rich social network, reducing depression and adhering to a Mediterranean diet;
3. Reducing brain inflammation by exercising, adhering to a Mediterranean diet and possibly the use of non-steroidal anti-inflammatories.

Less education is thought to result in less cognitive reserve in later life [2]. Cognitive reserve helps people maintain everyday function despite changes in brain pathology.

Exercise and physical activity in midlife are thought to have a neuroprotective effect through neurotransmitter action and reducing vascular risk. Observational studies have shown an inverse relationship between exercise and the risk of dementia [3,4].

Diabetes, high blood pressure and obesity are all vascular risk factors. In addition, changes in brain insulin in metabolic syndrome and diabetes may affect amyloid clearance and increase inflammation, impairing cognition [5].

Smoking is associated with cardiovascular disease and, in addition, contains neurotoxins which increase the risk of damage [6].

Depression has been associated with dementia in cohort studies [7] showing that the number of depressive episodes is linked to the risk of dementia. However, one study following people for up to 28 years [8] found that it was depression in the 10 years prior to the development of dementia that was relevant. It is thought depression increases dementia risk through its effect on stress hormones, neuronal growth factors and decreasing hippocampal volume.

Hearing loss has been recently recognized as a risk for cognitive impairment. Eleven cohort studies suggested that even mild levels of hearing loss in midlife are a risk for developing dementia in later life, although there are two studies which showed no increased risk. The mechanism is not yet clear [1].

Social isolation is associated with the risk of high blood pressure, heart disease and depression. It is thought that social isolation may result in cognitive inactivity, leading to faster cognitive decline and low mood [9].

Lead author of the recent Lancet report, Professor Gill Livingston, said they had considered risk factors with enough data to make meaningful conclusions and that it probably underestimated the importance of lifestyle in the prevention of dementia [1].

Fiona M. Jane

Women’s Health Research Program, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia

References

1. Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. Lancet 2017 July 19. Epub ahead of print
   http://www.ncbi.nlm.nih.gov/pubmed/28735855
2. Valenzuela MJ, Sachdev P. Brain reserve and dementia: a systematic review. Psychol Med 2006;36:441-54
   http://www.ncbi.nlm.nih.gov/pubmed/16207391
3. Sofi F, Valecchi D, Bacci D, et al. Physical activity and risk of cognitive decline: a meta-analysis of prospective studies. J Intern Med 2011;269:107-17
   http://www.ncbi.nlm.nih.gov/pubmed/20831630
4. Hamer M, Chida Y. Physical activity and risk of neurodegenerative disease: a systematic review of prospective evidence. Psychol Med 2009;39:3-11
   http://www.ncbi.nlm.nih.gov/pubmed/18570697
5. Yaffe K. Metabolic syndrome and cognitive disorders: is the sum greater than its parts? Alzheimer Dis Assoc Disord 2007;21:167-71
   http://www.ncbi.nlm.nih.gov/pubmed/17545744
6. Swan GE, Lessov-Schlaggar CN. The effects of tobacco smoke and nicotine on cognition and the brain. Neuropsychol Rev 2007;17:259-73
   http://www.ncbi.nlm.nih.gov/pubmed/17690985
7. Dotson VM, Beydoun MA, Zonderman AB. Recurrent depressive symptoms and the incidence of dementia and mild cognitive impairment. Neurology 2010;75:27-34
   http://www.ncbi.nlm.nih.gov/pubmed/20603482
8. Singh-Manoux A, Dugravot A, Fournier A, et al. Trajectories of depressive symptoms before diagnosis of dementia: a 28-year follow-up study. JAMA Psychiatry 2017;74:712-18
   http://www.ncbi.nlm.nih.gov/pubmed/28514478
9. Kuiper JS, Zuidersma M, Zuidema SU, et al. Social relationships and cognitive decline: a systematic review and meta-analysis of longitudinal cohort studies. Int J Epidemiol 2016;45:1169-206
   http://www.ncbi.nlm.nih.gov/pubmed/27272181