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- With increasing life expectancy there will be more dementia cases
- The risk factors for dementia appear to be the same as for cardiovascular disease
- Measures directed to prevent cardiovascular disease may also reduce the number of dementia cases
- Genes play a major role in dementia
Characteristics of dementia and different types
In rare cases, dementia may be caused by vitamin deficiency, chronic substance abuse, head injury, metabolic disease or other diseases. The vast majority of dementia cases are still associated with advanced age and this condition is known as age-related dementia.
Age-related dementia is an umbrella term for various dementia diseases including Alzheimer's disease, vascular dementia, Lewy-body dementia, frontotemporal dementia and other types. Age-related dementia rarely occurs before 70 years of age and usually not until 80 years, while almost every second person over 90 years has age-related dementia.
The condition develops slowly, often over several years and has no cure. The deterioration occurs faster as the disease progresses. If the person with dementia does not die of other causes, they will die of dementia after an estimated 10 years of disease.
A dementia diagnosis is usually based on various tests and discussions with the patient and family. An important part of the diagnosis is to exclude other possible causes of the cognitive impairment. In some cases it may also be important to rule out other mental disorders, since severe depression may sometimes manifest itself as a dementia-like condition.
Almost every fifth person will develop dementia during their lifetime
Calculations based on a large number of studies in Western Europe show a prevalence of 6.9 per cent among people over 59 years (Prince, 2013). The prevalence rises from 1.6 per cent in the age group 60-64 years to 43 per cent in the group over 89 years.
When these figures are compared with statistics for the age distribution in Norway, they show that about 1.5 per cent of the entire population suffers from dementia. Almost every fifth person will develop dementia during their lifetime (Seshadri, 2006).
The most common form of dementia is Alzheimer's disease which constitutes an estimated 60 per cent of all dementia (Qiu, 2007). Then comes vascular dementia (around 20 per cent) (Qiu, 2007) and dementia with Lewy bodies (10 per cent) (Zaccai, 2005). Estimates for frontotemporal dementia vary significantly, but this type barely constitutes more than 5 per cent (Bornebroek, 2004). Estimates of distribution of the various dementia types vary greatly.
Mixed type cases are very common and constitute perhaps nearly half of all dementia cases (Jelling, 2010). There are also unclear distinctions between the various dementia types, partly because symptoms for the various types overlap so strongly that it is difficult to give a definite diagnosis.
How much will the occurrence increase during the years to come?
It has been common to assume that about 70,000 people, or 1.4 per cent of the population, suffer from dementia in Norway (report, Norwegian Directorate of Health, 2007). This figure is mainly based on a single study from the Netherlands approximately 20 years ago and is uncertain (Ferri, 2005), but it tallies with the estimate of 1.5 per cent based on results from Western Europe (Prince, 2013). We do not have good data from Norway.
Calculations have shown that the expected increase in life expectancy in Norway will lead to over a doubling in the incidence of dementia from 2006 to 2050, if age-specific prevalence remains at current levels (Norwegian Directorate of Health, 2007). Other calculations have estimated a doubled incidence in Western Europe from 2001 to 2040 (Ferri, 2005). On a worldwide basis, it has been estimated that the incidence will double every 20 years (Reitz, 2011), while a more moderate estimate is a global tripling from 2001 to 2040 (Ferri, 2005).
However, this is the worst case projection. Some risk factors will probably be reduced through prevention, and a recent UK study has shown a decline in dementia prevalence from 8.3 to 6.5 per cent in the period from 1990 to 2010. The figures were adjusted because life expectancy was lower in 1990 (Matthews, 2013). In addition, a Danish study found clearly improved cognitive function among individuals aged 93-95 years over a decade (Christensen, 2013). Although preventive measures cannot prevent an increased prevalence of dementia due to higher life expectancy, the increase will probably be slowed a great deal.
Differences between different population groups
As mentioned, prevalence rises sharply with age, from an estimated 1.6 per cent in the 60-64 year age group to 43 per cent among people aged over 90 years (Prince, 2013). Almost every fifth person will die with dementia (Seshadri, 2006).
More women than men have dementia
A predominance of women among dementia cases can be partly attributed to higher life expectancy among women (SSB, 2014). However, prevalence is also higher among women than among men within the same age groups. The percentage difference between the sexes increases with age. Results from a European survey also show that while gender difference was small until 85 years of age, it was nearly 50 per cent higher among women than among men of the same age after this age (Lobo, 2000).
Socioeconomic differences in dementia
The incidence of dementia is higher among people with low education than among those with a higher education. Results from a meta-analysis of a large number of studies show that the risk increased by 80 per cent from the lowest to the highest education group for Alzheimer's and 60 per cent for other dementia types (Caamaño-Isorna, 2006). It is unclear how much is due to differences in lifestyle related to education. There are no statistics of possible differences related to different geographical areas.
Dementia prevalence appears to be highest in America and Europe, and lowest in Africa, according to calculations from an expert panel in 2010 (Sosa-Ortiz, 2012), see Figure 1. Another expert panel estimated similar, but slightly lower figures for 2001 (Qiu, 2007). The regional differences are probably related life expectancy differences (Qiu, 2007; Sosa-Ortiz, 2012) and there is little or no evidence to suggest significant differences in prevalence between western countries.
|Figure 1. Prevalence of dementia in different parts of the world (l-r Europe, America, Asia, Africa, world). Percentage of population over 60 years. Source: Sosa-Ortiz, 2012.|
An international expert panel concluded in 2010 that there is no completely reliable knowledge of modifiable risk factors for dementia but that promising research points out probable factors (Plassman, 2010). New results have been reached but knowledge about specific causal factors is uncertain.
To some extent causal factors assumed to have contributed to dementia are related to choice of diagnosis. For example, if the patient has a history of high blood pressure and is believed to have had a stroke, this is an indication that the condition is vascular dementia. Using potential risk factors to determine the diagnosis complicates the research into which factors actually lead to increased risk for the various dementia types.
Nevertheless, we must assume that since vascular dementia is caused by clogging of blood vessels, the risk factors are to some extent the same as for other cardiovascular diseases, particularly stroke. These risk factors include high blood pressure, high cholesterol, diabetes, inflammation and recurrent infections, hormone replacements, smoking, excessive alcohol consumption, unhealthy diet, physical inactivity and obesity (Plassman, 2010 Grysiewicz, 2008).
Since many dementia cases are in reality mixed types, the risk factors for vascular dementia also apply for a large proportion of dementia cases, including mixed types diagnosed as Alzheimer's disease. Some research results have even shown that "pure" Alzheimer’s patients also seem to be significantly affected by cardiovascular risk factors (Tolppanen, 2012). Perhaps this type of dementia could also be considered as a cardiovascular disease? (Tolppanen, 2012).
Apart from age, a variant of the apolipoprotein gene (ApoE, allele ε4 on chromosome 19) is the strongest known risk factor for Alzheimer's disease. An estimated 40-80 per cent of patients with Alzheimer’s inherited this variant from at least one of their parents. If the gene is transferred from one parent, the risk is tripled and if the gene is inherited from both parents, the risk increases 11-fold (Schipper, 2011).
ApoE4 causes large accumulation of beta-amyloid in the brain before Alzheimer’s symptoms arise (Polvikoski, 1995). So far, ApoE4 has been primarily linked to Alzheimer's. However, the results described in a review article indicate that this gene is an equally strong risk factor for vascular dementia (Liu, 2012). In addition to ApoE4, there are about 20 other genes coding for dementia, but none with equally strong efficacy (Lambert, 2013).
Other probable risk factors for dementia in general are depression and lack of cognitive training and stimulation (Plassman, 2010). There is also an increased risk linked to a lower education (Norwegian Directorate of Health, 2007).
Twin studies show that genes are slightly more important than general environmental factors as an explanation for Alzheimer’s (Bergem, 1997; Gatz, 2006). There are no corresponding research results for other dementia types.
Consequences of dementia
Dementia patients experience loss of cognitive functions, and will eventually die from, or with, the disease.
For close contacts, especially spouses or children, the disease can be a huge burden. The experience of gradually losing someone close is a painful and often lengthy process. In addition, the care burden is often heavy and tiring.
Fortunately, from a preventive standpoint it seems that the road to a dementia-free life is about the same as to good health in general. Since the risk of dementia increases with increased clogging of the arteries, interventions aimed at reducing the incidence of cardiovascular disease probably also protect against dementia. Examples include increased physical activity, less smoking and a healthy diet.
Types of dementia
Alzheimer's disease is associated with errors in protein breakdown, so that beta-amyloid is deposited in the brain outside the nerve cells, particularly in the temporal lobe. These plaques damage the surrounding cells. The disease progresses in different stages.
Vascular dementia is caused by loss of blood supply to part of the brain so brain cells die. This is most commonly caused by clogged blood vessels that have led to repeated heart attacks and strokes or hardening of the arteries (arteriosclerosis) which gradually restricts blood flow. This form of dementia typically progresses more incrementally than Alzheimer's disease and begins more abruptly.
Lewy-body dementia is a condition that resembles Alzheimer's disease and is perhaps a subset of this disease. Patients experience stiffness in the arms and legs and psychotic symptoms with periodic visual hallucinations, delusions and suspicion, with the symptoms varying from day to day or from hour to hour.
Frontotemporal dementia is related to damage to the frontal lobe of the brain. It often arises earlier than other forms of dementia, often before 70 years of age. Typical of this disease is change of personality, loss of social inhibitions, flattening of emotional responses, lack of empathy and preoccupation with satisfying their own needs. The patients are usually unaware of their own illness.
Bergem, A. L., K. Engedal and E. Kringlen (1997). The role of heredity in late-onset Alzheimer disease and vascular dementia. A twin study. Arch Gen Psychiatry 54(3): 264-270.
Bornebroek, M. and M. M. B. Breteler (2004). Epidemiology of non-AD dementias. Clinical Neuroscience Research 3(6): 349-361.
Caamano-Isorna, F., M. Corral, A. Montes-Martinez and B. Takkouche (2006). Education and dementia: a meta-analytic study. Neuroepidemiology 26(4): 226-232.
Christensen, K., M. Thinggaard, A. Oksuzyan, T. Steenstrup, K. Andersen-Ranberg, B. Jeune, M. McGue and J. W. Vaupel (2013). Physical and cognitive functioning of people older than 90 years: a comparison of two Danish cohorts born 10 years apart. Lancet 382(9903): 1507-1513.
European Alzheimer's Disease, I., Genetic, D. Environmental Risk in Alzheimer's, C. Alzheimer's Disease Genetic, H. Cohorts for and E. Aging Research in Genomic (2013). Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease. Nat Genet 45(12): 1452-1458.
Ferri, C. P., M. Prince, C. Brayne, H. Brodaty, L. Fratiglioni, M. Ganguli, K. Hall, K. Hasegawa, H. Hendrie, Y. Huang, A. Jorm, C. Mathers, P. R. Menezes, E. Rimmer, M. Scazufca and I. Alzheimer's Disease (2005). Global prevalence of dementia: a Delphi consensus study. Lancet 366(9503): 2112-2117.
Gatz, M., C. A. Reynolds, L. Fratiglioni, B. Johansson, J. A. Mortimer, S. Berg, A. Fiske and N. L. Pedersen (2006). Role of genes and environments for explaining Alzheimer disease. Arch Gen Psychiatry 63(2): 168-174.
Grysiewicz, R. A., K. Thomas and D. K. Pandey (2008). Epidemiology of ischemic and hemorrhagic stroke: incidence, prevalence, mortality, and risk factors. Neurol Clin 26(4): 871-895, vii.
Jellinger, K. A. and J. Attems (2010). Prevalence of dementia disorders in the oldest-old: an autopsy study. Acta Neuropathol 119(4): 421-433.
Liu, X., L. Li, F. Liu, S. Deng, R. Zhu, Q. Li and Z. He (2012). ApoE gene polymorphism and vascular dementia in Chinese population: a meta-analysis. J Neural Transm 119(3): 387-394.
Lobo, A., L. J. Launer, L. Fratiglioni, K. Andersen, A. Di Carlo, M. M. Breteler, J. R. Copeland, J. F. Dartigues, C. Jagger, J. Martinez-Lage, H. Soininen and A. Hofman (2000). Prevalence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group. Neurology 54(11 Suppl 5): S4-9.
Matthews, F. E., A. Arthur, L. E. Barnes, J. Bond, C. Jagger, L. Robinson, C. Brayne, F. Medical Research Council Cognitive and C. Ageing (2013). A two-decade comparison of prevalence of dementia in individuals aged 65 years and older from three geographical areas of England: results of the Cognitive Function and Ageing Study I and II. Lancet 382(9902): 1405-1412.
Ott, A., M. M. Breteler, F. van Harskamp, J. J. Claus, T. J. van der Cammen, D. E. Grobbee and A. Hofman (1995). Prevalence of Alzheimer's disease and vascular dementia: association with education. The Rotterdam study. BMJ 310(6985): 970-973.
Polvikoski, T., R. Sulkava, M. Haltia, K. Kainulainen, A. Vuorio, A. Verkkoniemi, L. Niinisto, P. Halonen and K. Kontula (1995). Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein. N Engl J Med 333(19): 1242-1247.
Qiu, C., D. De Ronchi and L. Fratiglioni (2007). The epidemiology of the dementias: an update. Curr Opin Psychiatry 20(4): 380-385.
Reitz, C., C. Brayne and R. Mayeux (2011). Epidemiology of Alzheimer disease. Nat Rev Neurol 7(3): 137-152.
Schipper, H. M. (2011). Apolipoprotein E: implications for AD neurobiology, epidemiology and risk assessment. Neurobiol Aging 32(5): 778-790.
Sosa-Ortiz, A. L., I. Acosta-Castillo and M. J. Prince (2012). Epidemiology of dementias and Alzheimer's disease. Arch Med Res 43(8): 600-608.
Norwegian Directorate of Health, 2007. Glemsk, men ikke glemt!: om dagens situasjon og framtidas utfordringer for å styrke tjenestetilbudet til personer med demens. (Forgetful but not forgotten - report in Norwegian only)
Statistics Norway (SSB). Statistic bank, available from SSB. Extracted June 2014.
Tolppanen, A. M., A. Solomon, H. Soininen and M. Kivipelto (2012). Midlife vascular risk factors and Alzheimer's disease: evidence from epidemiological studies. J Alzheimers Dis 32(3): 531-540.
Zaccai, J., C. McCracken and C. Brayne (2005). A systematic review of prevalence and incidence studies of dementia with Lewy bodies. Age Ageing 34(6): 561-566.