Van Gool discusses a new study that found that the prevalence of dementia and severe cognitive impairment in the year before death rises steeply with age

Van Gool, Willem A

PLoS Medicine

English

PubMed

Gool, W.A. van

International Migration, Integration and Social Cohesion online publications

UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl)UvA-DARE (Digital Academic Repository)Can we prevent, delay, or shorten the course of dementia?Gool, W.A. vanDOI10.1371/journal.pmed.0030430Publication date2006Published inPLoS MedicineLink to publicationCitation for published version (APA):Gool, W. A. V. (2006). Can we prevent, delay, or shorten the course of dementia? PLoSMedicine, 3(10), 1717-1718. https://doi.org/10.1371/journal.pmed.0030430General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s)and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an opencontent license (like Creative Commons).Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, pleaselet the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the materialinaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letterto: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. Youwill be contacted as soon as possible.Download date:10 Mar 2023PLoS Medicine  |  www.plosmedicine.org 1717 Perspectives October 2006  |  Volume 3  |  Issue 10  |  e430 “You already know how it ends when you are born”, my mother said in sorrow after my father died. And she is not even medically qualifi ed. Should we extend this common wisdom on the realities of old age towards the development of dementia? In other words, is dementia a curse that is inescapably linked to old age?  A New Study on Dementia before Death In a new study in  PLoS Medicine , Carol Brayne and colleagues show that in a large population sample, the prevalence of dementia and severe cognitive impairment in the year before death rises steeply with age [1]. The researchers found that the prevalence of dementia in the year before death is up to 40%–60% in those over 90 years of age. They also found that nearly 80% of those dying over 95 years of age suffered from moderate or more severe cognitive impairment.  The researchers examined whether higher levels of education and higher social class (proxies for a healthy lifestyle, e.g., taking exercise and not smoking) protected people from dementia by the time they died. While they did fi nd such a protective effect, the size of this effect was small: higher social class reduced the risk of dying with dementia by only 2%, and higher levels of education reduced the risk by only 7%.  Policy and Clinical Implications These fi gures are important and sobering for policy makers and for those who believe that dementia is preventable. It is diffi cult to envisage preventive measures that would effectively counteract the profound effects of increasing age on the risk of dementia. As populations age, the burden of dementia will increase, and societies should be prepared for large numbers of elderly patients with dementia. Wishful thinking on prevention of dementia should not defer from the societal investments that are required for providing high quality care for these patients. That is an important message for policy makers and health-care workers alike.  While acknowledging both the methodological rigor of Brayne and colleagues’ analysis and the sobering nature of their data, it is important to note that their dataset does allow for slightly more hopeful interpretations. First, the authors’ strong emphasis on the large proportion of patients with dementia  at the time of death must not let us forget about the importance of the age of onset or the duration of dementia. Their fi gures do not preclude the possibility that substantial gains might be made by delaying the onset of dementia, shortening the period with dementia, or both (Figure 1). Such scenarios, which would not change the total number of patients suffering from dementia in the period before death, could yield enormous benefi ts in terms of alleviating suffering at younger ages and reducing the burden for families and other informal caregivers.  Second, the observational nature of the present study limits its interpretation in terms of cause and effects, especially with respect to the small effects of potential protective factors. The important role of cardiovascular risk factors for dementia and more specifi cally for Alzheimer disease has been recognized  Can We Prevent, Delay, or Shorten the Course of Dementia? Willem A. Van Gool Funding: The author received no specifi c funding for this article.  Competing Interests: The author is Principal Investigator of pre-DIVA (“Prevention of dementia by intensive vascular care”, ISRCTN #29711771), a study of primary prevention of dementia. Citation: Van Gool WA (2006) Can We Prevent, Delay, or Shorten the Course of Dementia? PLoS Med 3(10): e430. DOI: 10.1371/journal.pmed.0030430 DOI: 10.1371/journal.pmed.0030430 Copyright: © 2006 Willem A. Van Gool. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.  Willem A. Van Gool is a professor in the Department of Neurology, Academic Medical Centre, Amsterdam, Netherlands. E-mail: w.a.vangool@amc.uva.nl The Perspectives section is for experts to discuss the clinical practice or public health implications of a published article that is freely available online.DOI: 10.1371/journal.pmed.0030430.g001 Figure 1.  Curves Depicting Severity of Dementia Depending on Age The solid line gives an estimate of a present individual trajectory. Broken lines illustrate the potential benefi t of (A) postponing and shortening the episode with dementia, (B) delaying dementia while reaching a higher age, or (C) preventing dementia. PLoS Medicine  |  www.plosmedicine.org 1718for almost ten years [2]. This has fuelled the hope that at least some components of dementia may be amenable to preventive measures. Both observational and trial data suggest that treatment of hypertension does indeed protect against dementia, and the same may hold for interventions directed against obesity, smoking, lack of exercise, and glucose intolerance [3–10].  As acknowledged by Brayne and colleagues, stratifi cation according to educational levels and social class—as proxies for the level of cardiovascular prevention—is not very strong. Physical fi tness, body weight, smoking behaviour, blood pressure, and glucose intolerance might have been better indicators, but even then observational studies like theirs, which can be biased by confounding factors, may fail to defi ne the potential for vascular prevention of dementia.  The Need for Randomised Controlled Trials Only properly designed randomised controlled trials of suffi cient power and suffi ciently long follow up can convincingly defi ne the window of opportunity for prevention of dementia. Such studies, which will be a major undertaking, can also document the precise effects of risks that may compete with the onset of dementia. Delaying the onset of dementia by, say, six to eight years may unmask other diseases in the elderly such as ischemic heart disease or cancer, which would have gone undetected if the dementia had not been delayed. The effects of these competing risks on survival may eventually determine if delaying the onset of dementia may ultimately result in prevention of dementia (Figure 1).  Individuals who develop dementia at the age of 75 or 85 years may differ in more respects than just the tendency to develop dementia. Therefore, in the absence of randomisation and without an intervention that protects individuals who would have developed dementia at a given age, observational studies can never precisely defi ne the effects of risks that may compete with the onset of dementia.  Direct studies of the benefi cial and adverse effects of preventive measures are required irrespective of their target, being either ß-amyloid accumulation in the brain or vascular brain damage. At least one such study is now under way (“Prevention of dementia by intensive vascular care [pre-DIVA]”, ISRCTN #29711771). Because of the long follow up that is required in studies of primary prevention, it will be several years before we will know if the one-way funnel leading towards nursing home placement can be turned into a freeway leading to a life free from dementia at old age.   References 1. Brayne C, Gao L, Dewey M, Matthews FE, Medical Research Council Cognitive Function and Ageing Study Investigators (2006) Dementia before death in ageing societies—The promise of prevention and the reality. PLoS Med 3(9): e397. DOI: 10.1371/journal.pmed.0030397 2. Hofman A, Ott A, Breteler MM, Bots ML, Slooter AJ, et al. (1997) Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer’s disease in the Rotterdam Study. Lancet 349: 151–154. 3. Forette F, Seux ML, Staessen JA, Thijs L, Babarskiene MR, et al. (2002) The prevention of dementia with antihypertensive treatment: New evidence from the Systolic Hypertension in Europe (Syst-Eur) study. Arch Intern Med 162: 2046–2052. 4. Khachaturian AS, Zandi PP, Lyketsos CG, Hayden KM, Skoog I, et al. (2006) Antihypertensive medication use and incident Alzheimer disease: The Cache County Study. Arch Neurol 63: 686–692. 5. Ott A, Andersen K, Dewey ME, Letenneur L, Brayne C, et al. (2004) Effect of smoking on global cognitive function in nondemented elderly. Neurology 62: 920–924. 6. Nicolls MR (2004) The clinical and biological relationship between Type II diabetes mellitus and Alzheimer’s disease. Curr Alzheimer Res 1: 47–54. 7. Whitmer RA, Gunderson EP, Barrett-Connor E, Quesenberry CP Jr, Yaffe K (2005) Obesity in middle age and future risk of dementia: A 27 year longitudinal population based study. BMJ 330: 1360. 8. Kivipelto M, Ngandu T, Fratiglioni L, Viitanen M, Kåreholt I, et al. (2005) Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch Neurol 62: 1556–1560. 9. Weuve J, Kang JH, Manson JE, Breteler MM, Ware JH, et al. (2004) Physical activity, including walking, and cognitive function in older women. JAMA 292: 1454–1461. 10. Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, et al. (2004) Walking and dementia in physically capable elderly men. JAMA 292: 1447–1453. October 2006  |  Volume 3  |  Issue 10  |  e430

Can we prevent, delay, or shorten the course of dementia?

van Gool, Willem A.

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Willem A Van Gool

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Van Gool Willem A

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Can We Prevent, Delay, or Shorten the Course of Dementia?

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Can we prevent, delay, or shorten the course of dementia?
Gool, W.A. van
Published in:
PLoS Medicine
DOI:
10.1371/journal.pmed.0030430
Link to publication
Citation for published version (APA):
Gool, W. A. V. (2006). Can we prevent, delay, or shorten the course of dementia? PLoS Medicine, 3(10), 1717-
1718. https://doi.org/10.1371/journal.pmed.0030430
General rights
It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s),
other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons).
Disclaimer/Complaints regulations
If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating
your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask
the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam,
The Netherlands. You will be contacted as soon as possible.
Download date: 04 Feb 2021
PLoS Medicine  |  www.plosmedicine.org 1717
 Perspectives 
October 2006  |  Volume 3  |  Issue 10  |  e430
 “You already know how it ends when you are born”, my mother said in sorrow after 
my father died. And she is not even 
medically qualifi ed. Should we extend 
this common wisdom on the realities 
of old age towards the development of 
dementia? In other words, is dementia 
a curse that is inescapably linked to old 
age? 
 A New Study on Dementia before 
Death
 In a new study in  PLoS Medicine , Carol 
Brayne and colleagues show that 
in a large population sample, the 
prevalence of dementia and severe 
cognitive impairment in the year before 
death rises steeply with age [1]. The 
researchers found that the prevalence 
of dementia in the year before death is 
up to 40%–60% in those over 90 years 
of age. They also found that nearly 
80% of those dying over 95 years of age 
suffered from moderate or more severe 
cognitive impairment. 
 The researchers examined whether 
higher levels of education and higher 
social class (proxies for a healthy 
lifestyle, e.g., taking exercise and not 
smoking) protected people from 
dementia by the time they died. While 
they did fi nd such a protective effect, 
the size of this effect was small: higher 
social class reduced the risk of dying 
with dementia by only 2%, and higher 
levels of education reduced the risk by 
only 7%. 
 Policy and Clinical Implications
 These fi gures are important and 
sobering for policy makers and for 
those who believe that dementia is 
preventable. It is diffi cult to envisage 
preventive measures that would 
effectively counteract the profound 
effects of increasing age on the risk 
of dementia. As populations age, the 
burden of dementia will increase, 
and societies should be prepared for 
large numbers of elderly patients 
with dementia. Wishful thinking on 
prevention of dementia should not 
defer from the societal investments 
that are required for providing high 
quality care for these patients. That is 
an important message for policy makers 
and health-care workers alike. 
 While acknowledging both the 
methodological rigor of Brayne and 
colleagues’ analysis and the sobering 
nature of their data, it is important to 
note that their dataset does allow for 
slightly more hopeful interpretations. 
First, the authors’ strong emphasis on 
the large proportion of patients with 
dementia  at the time of death must not 
let us forget about the importance 
of the age of onset or the duration 
of dementia. Their fi gures do not 
preclude the possibility that substantial 
gains might be made by delaying the 
onset of dementia, shortening the 
period with dementia, or both (Figure 
1). Such scenarios, which would not 
change the total number of patients 
suffering from dementia in the period 
before death, could yield enormous 
benefi ts in terms of alleviating suffering 
at younger ages and reducing the 
burden for families and other informal 
caregivers. 
 Second, the observational 
nature of the present study limits 
its interpretation in terms of cause 
and effects, especially with respect 
to the small effects of potential 
protective factors. The important 
role of cardiovascular risk factors for 
dementia and more specifi cally for 
Alzheimer disease has been recognized 
 Can We Prevent, Delay, or Shorten 
the Course of Dementia? 
Willem A. Van Gool
 Funding: The author received no specifi c funding for 
this article. 
 Competing Interests: The author is Principal 
Investigator of pre-DIVA (“Prevention of dementia by 
intensive vascular care”, ISRCTN #29711771), a study 
of primary prevention of dementia.
 Citation: Van Gool WA (2006) Can We Prevent, Delay, 
or Shorten the Course of Dementia? PLoS Med 3(10): 
e430. DOI: 10.1371/journal.pmed.0030430
 DOI: 10.1371/journal.pmed.0030430
 Copyright: © 2006 Willem A. Van Gool. This is an 
open-access article distributed under the terms 
of the Creative Commons Attribution License, 
which permits unrestricted use, distribution, and 
reproduction in any medium, provided the original 
author and source are credited. 
 Willem A. Van Gool is a professor in the Department 
of Neurology, Academic Medical Centre, Amsterdam, 
Netherlands. E-mail: w.a.vangool@amc.uva.nl 
The Perspectives section is for experts to discuss the 
clinical practice or public health implications of a 
published article that is freely available online.
DOI: 10.1371/journal.pmed.0030430.g001
 Figure 1.  Curves Depicting Severity of Dementia Depending on Age
 The solid line gives an estimate of a present individual trajectory. Broken lines illustrate the 
potential benefi t of (A) postponing and shortening the episode with dementia, (B) delaying 
dementia while reaching a higher age, or (C) preventing dementia. 
PLoS Medicine  |  www.plosmedicine.org 1718
for almost ten years [2]. This has 
fuelled the hope that at least some 
components of dementia may be 
amenable to preventive measures. Both 
observational and trial data suggest 
that treatment of hypertension does 
indeed protect against dementia, and 
the same may hold for interventions 
directed against obesity, smoking, lack 
of exercise, and glucose intolerance 
[3–10]. 
 As acknowledged by Brayne and 
colleagues, stratifi cation according to 
educational levels and social class—as 
proxies for the level of cardiovascular 
prevention—is not very strong. 
Physical fi tness, body weight, smoking 
behaviour, blood pressure, and glucose 
intolerance might have been better 
indicators, but even then observational 
studies like theirs, which can be biased 
by confounding factors, may fail 
to defi ne the potential for vascular 
prevention of dementia. 
 The Need for Randomised 
Controlled Trials
 Only properly designed randomised 
controlled trials of suffi cient power 
and suffi ciently long follow up can 
convincingly defi ne the window 
of opportunity for prevention of 
dementia. Such studies, which will be a 
major undertaking, can also document 
the precise effects of risks that may 
compete with the onset of dementia. 
Delaying the onset of dementia by, say, 
six to eight years may unmask other 
diseases in the elderly such as ischemic 
heart disease or cancer, which would 
have gone undetected if the dementia 
had not been delayed. The effects 
of these competing risks on survival 
may eventually determine if delaying 
the onset of dementia may ultimately 
result in prevention of dementia 
(Figure 1). 
 Individuals who develop dementia at 
the age of 75 or 85 years may differ in 
more respects than just the tendency 
to develop dementia. Therefore, in 
the absence of randomisation and 
without an intervention that protects 
individuals who would have developed 
dementia at a given age, observational 
studies can never precisely defi ne the 
effects of risks that may compete with 
the onset of dementia. 
 Direct studies of the benefi cial and 
adverse effects of preventive measures 
are required irrespective of their target, 
being either ß-amyloid accumulation in 
the brain or vascular brain damage. At 
least one such study is now under way 
(“Prevention of dementia by intensive 
vascular care [pre-DIVA]”, ISRCTN 
#29711771). Because of the long 
follow up that is required in studies of 
primary prevention, it will be several 
years before we will know if the one-way 
funnel leading towards nursing home 
placement can be turned into a freeway 
leading to a life free from dementia at 
old age.  
 References
 1. Brayne C, Gao L, Dewey M, Matthews FE, 
Medical Research Council Cognitive Function 
and Ageing Study Investigators (2006) 
Dementia before death in ageing societies—
The promise of prevention and the reality. 
PLoS Med 3(9): e397. DOI: 10.1371/journal.
pmed.0030397
 2. Hofman A, Ott A, Breteler MM, Bots ML, 
Slooter AJ, et al. (1997) Atherosclerosis, 
apolipoprotein E, and prevalence of dementia 
and Alzheimer’s disease in the Rotterdam 
Study. Lancet 349: 151–154.
 3. Forette F, Seux ML, Staessen JA, Thijs L, 
Babarskiene MR, et al. (2002) The prevention 
of dementia with antihypertensive treatment: 
New evidence from the Systolic Hypertension 
in Europe (Syst-Eur) study. Arch Intern Med 
162: 2046–2052.
 4. Khachaturian AS, Zandi PP, Lyketsos 
CG, Hayden KM, Skoog I, et al. (2006) 
Antihypertensive medication use and incident 
Alzheimer disease: The Cache County Study. 
Arch Neurol 63: 686–692.
 5. Ott A, Andersen K, Dewey ME, Letenneur L, 
Brayne C, et al. (2004) Effect of smoking on 
global cognitive function in nondemented 
elderly. Neurology 62: 920–924.
 6. Nicolls MR (2004) The clinical and biological 
relationship between Type II diabetes mellitus 
and Alzheimer’s disease. Curr Alzheimer Res 1: 
47–54.
 7. Whitmer RA, Gunderson EP, Barrett-Connor 
E, Quesenberry CP Jr, Yaffe K (2005) Obesity 
in middle age and future risk of dementia: A 27 
year longitudinal population based study. BMJ 
330: 1360.
 8. Kivipelto M, Ngandu T, Fratiglioni L, Viitanen 
M, Kåreholt I, et al. (2005) Obesity and 
vascular risk factors at midlife and the risk of 
dementia and Alzheimer disease. Arch Neurol 
62: 1556–1560.
 9. Weuve J, Kang JH, Manson JE, Breteler 
MM, Ware JH, et al. (2004) Physical activity, 
including walking, and cognitive function in 
older women. JAMA 292: 1454–1461.
 10. Abbott RD, White LR, Ross GW, Masaki KH, 
Curb JD, et al. (2004) Walking and dementia 
in physically capable elderly men. JAMA 292: 
1447–1453. 
October 2006  |  Volume 3  |  Issue 10  |  e430


UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl)UvA-DARE (Digital Academic Repository)Can we prevent, delay, or shorten the course of dementia?Gool, W.A. vanDOI10.1371/journal.pmed.0030430Publication date2006Published inPLoS MedicineLink to publicationCitation for published version (APA):Gool, W. A. V. (2006). Can we prevent, delay, or shorten the course of dementia? PLoSMedicine, 3(10), 1717-1718. https://doi.org/10.1371/journal.pmed.0030430General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s)and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an opencontent license (like Creative Commons).Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, pleaselet the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the materialinaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letterto: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. Youwill be contacted as soon as possible.Download date:10 Nov 2022PLoS Medicine  |  www.plosmedicine.org 1717 Perspectives October 2006  |  Volume 3  |  Issue 10  |  e430 “You already know how it ends when you are born”, my mother said in sorrow after my father died. And she is not even medically qualifi ed. Should we extend this common wisdom on the realities of old age towards the development of dementia? In other words, is dementia a curse that is inescapably linked to old age?  A New Study on Dementia before Death In a new study in  PLoS Medicine , Carol Brayne and colleagues show that in a large population sample, the prevalence of dementia and severe cognitive impairment in the year before death rises steeply with age [1]. The researchers found that the prevalence of dementia in the year before death is up to 40%–60% in those over 90 years of age. They also found that nearly 80% of those dying over 95 years of age suffered from moderate or more severe cognitive impairment.  The researchers examined whether higher levels of education and higher social class (proxies for a healthy lifestyle, e.g., taking exercise and not smoking) protected people from dementia by the time they died. While they did fi nd such a protective effect, the size of this effect was small: higher social class reduced the risk of dying with dementia by only 2%, and higher levels of education reduced the risk by only 7%.  Policy and Clinical Implications These fi gures are important and sobering for policy makers and for those who believe that dementia is preventable. It is diffi cult to envisage preventive measures that would effectively counteract the profound effects of increasing age on the risk of dementia. As populations age, the burden of dementia will increase, and societies should be prepared for large numbers of elderly patients with dementia. Wishful thinking on prevention of dementia should not defer from the societal investments that are required for providing high quality care for these patients. That is an important message for policy makers and health-care workers alike.  While acknowledging both the methodological rigor of Brayne and colleagues’ analysis and the sobering nature of their data, it is important to note that their dataset does allow for slightly more hopeful interpretations. First, the authors’ strong emphasis on the large proportion of patients with dementia  at the time of death must not let us forget about the importance of the age of onset or the duration of dementia. Their fi gures do not preclude the possibility that substantial gains might be made by delaying the onset of dementia, shortening the period with dementia, or both (Figure 1). Such scenarios, which would not change the total number of patients suffering from dementia in the period before death, could yield enormous benefi ts in terms of alleviating suffering at younger ages and reducing the burden for families and other informal caregivers.  Second, the observational nature of the present study limits its interpretation in terms of cause and effects, especially with respect to the small effects of potential protective factors. The important role of cardiovascular risk factors for dementia and more specifi cally for Alzheimer disease has been recognized  Can We Prevent, Delay, or Shorten the Course of Dementia? Willem A. Van Gool Funding: The author received no specifi c funding for this article.  Competing Interests: The author is Principal Investigator of pre-DIVA (“Prevention of dementia by intensive vascular care”, ISRCTN #29711771), a study of primary prevention of dementia. Citation: Van Gool WA (2006) Can We Prevent, Delay, or Shorten the Course of Dementia? PLoS Med 3(10): e430. DOI: 10.1371/journal.pmed.0030430 DOI: 10.1371/journal.pmed.0030430 Copyright: © 2006 Willem A. Van Gool. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.  Willem A. Van Gool is a professor in the Department of Neurology, Academic Medical Centre, Amsterdam, Netherlands. E-mail: w.a.vangool@amc.uva.nl The Perspectives section is for experts to discuss the clinical practice or public health implications of a published article that is freely available online.DOI: 10.1371/journal.pmed.0030430.g001 Figure 1.  Curves Depicting Severity of Dementia Depending on Age The solid line gives an estimate of a present individual trajectory. Broken lines illustrate the potential benefi t of (A) postponing and shortening the episode with dementia, (B) delaying dementia while reaching a higher age, or (C) preventing dementia. PLoS Medicine  |  www.plosmedicine.org 1718for almost ten years [2]. This has fuelled the hope that at least some components of dementia may be amenable to preventive measures. Both observational and trial data suggest that treatment of hypertension does indeed protect against dementia, and the same may hold for interventions directed against obesity, smoking, lack of exercise, and glucose intolerance [3–10].  As acknowledged by Brayne and colleagues, stratifi cation according to educational levels and social class—as proxies for the level of cardiovascular prevention—is not very strong. Physical fi tness, body weight, smoking behaviour, blood pressure, and glucose intolerance might have been better indicators, but even then observational studies like theirs, which can be biased by confounding factors, may fail to defi ne the potential for vascular prevention of dementia.  The Need for Randomised Controlled Trials Only properly designed randomised controlled trials of suffi cient power and suffi ciently long follow up can convincingly defi ne the window of opportunity for prevention of dementia. Such studies, which will be a major undertaking, can also document the precise effects of risks that may compete with the onset of dementia. Delaying the onset of dementia by, say, six to eight years may unmask other diseases in the elderly such as ischemic heart disease or cancer, which would have gone undetected if the dementia had not been delayed. The effects of these competing risks on survival may eventually determine if delaying the onset of dementia may ultimately result in prevention of dementia (Figure 1).  Individuals who develop dementia at the age of 75 or 85 years may differ in more respects than just the tendency to develop dementia. Therefore, in the absence of randomisation and without an intervention that protects individuals who would have developed dementia at a given age, observational studies can never precisely defi ne the effects of risks that may compete with the onset of dementia.  Direct studies of the benefi cial and adverse effects of preventive measures are required irrespective of their target, being either ß-amyloid accumulation in the brain or vascular brain damage. At least one such study is now under way (“Prevention of dementia by intensive vascular care [pre-DIVA]”, ISRCTN #29711771). Because of the long follow up that is required in studies of primary prevention, it will be several years before we will know if the one-way funnel leading towards nursing home placement can be turned into a freeway leading to a life free from dementia at old age.   References 1. Brayne C, Gao L, Dewey M, Matthews FE, Medical Research Council Cognitive Function and Ageing Study Investigators (2006) Dementia before death in ageing societies—The promise of prevention and the reality. PLoS Med 3(9): e397. DOI: 10.1371/journal.pmed.0030397 2. Hofman A, Ott A, Breteler MM, Bots ML, Slooter AJ, et al. (1997) Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer’s disease in the Rotterdam Study. Lancet 349: 151–154. 3. Forette F, Seux ML, Staessen JA, Thijs L, Babarskiene MR, et al. (2002) The prevention of dementia with antihypertensive treatment: New evidence from the Systolic Hypertension in Europe (Syst-Eur) study. Arch Intern Med 162: 2046–2052. 4. Khachaturian AS, Zandi PP, Lyketsos CG, Hayden KM, Skoog I, et al. (2006) Antihypertensive medication use and incident Alzheimer disease: The Cache County Study. Arch Neurol 63: 686–692. 5. Ott A, Andersen K, Dewey ME, Letenneur L, Brayne C, et al. (2004) Effect of smoking on global cognitive function in nondemented elderly. Neurology 62: 920–924. 6. Nicolls MR (2004) The clinical and biological relationship between Type II diabetes mellitus and Alzheimer’s disease. Curr Alzheimer Res 1: 47–54. 7. Whitmer RA, Gunderson EP, Barrett-Connor E, Quesenberry CP Jr, Yaffe K (2005) Obesity in middle age and future risk of dementia: A 27 year longitudinal population based study. BMJ 330: 1360. 8. Kivipelto M, Ngandu T, Fratiglioni L, Viitanen M, Kåreholt I, et al. (2005) Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch Neurol 62: 1556–1560. 9. Weuve J, Kang JH, Manson JE, Breteler MM, Ware JH, et al. (2004) Physical activity, including walking, and cognitive function in older women. JAMA 292: 1454–1461. 10. Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, et al. (2004) Walking and dementia in physically capable elderly men. JAMA 292: 1447–1453. October 2006  |  Volume 3  |  Issue 10  |  e430

Antihypertensive medication use and incident Alzheimer disease: The Cache County Study.

Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer’s disease in the Rotterdam Study.

Effect of smoking on global cognitive function in nondemented elderly.

Medical Research Council Cognitive Function and Ageing Study Investigators

Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease.

Obesity in middle age and future risk of dementia: A 27 year longitudinal population based study.

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